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  • 2010-2014  (1)
  • 1990-1994  (150,145)
  • 1992  (150,145)
Source
Material
Years
Year
Person/Organisation
Keywords
Language
  • 1
    Electronic Resource
    Electronic Resource
    A measurement of τ polarization in Z^0 decays (1992-8977)
    Amsterdam : Elsevier
    Physics Letters B 294 (1992), S. 466-478 
    Details
    ISSN: 0370-2693
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0370-2693(92)91549-O
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    Paper (German National Licenses)
    Fulltext
  • 2
    Book
    Book
    Computing : archives for informatics and numerical computation; Supplementum (1977-2003)
    Wien [u.a.] :Springer, ; 1.1977 - 16.2003; damit Ersch. eingest.
    Details
    Title: Computing : archives for informatics and numerical computation; Supplementum
    Publisher: Wien [u.a.] :Springer,
    Year of publication: 1977-2003
    Dates of Publication: 1.1977 - 16.2003; damit Ersch. eingest.
    Type of Medium: Book
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  • 3
    Journal/Serial
    Journal/Serial
    SIGBIO newsletter / (from 1969-2001)
    New York, NY :ACM, ; 1.1969 - 7.1975/76; N.S. 1.1976 - 21.2001,1; damit Ersch. eingest.
    Details
    Title: SIGBIO newsletter /
    Author: Association for Computing Machinery / Special Interest Group on Biomedical Computing
    Publisher: New York, NY :ACM,
    Year of publication: 1969-2001
    Dates of Publication: 1.1969 - 7.1975/76; N.S. 1.1976 - 21.2001,1; damit Ersch. eingest.
    ISSN: 0163-5697
    Type of Medium: Journal/Serial
    Language: Undetermined
    Parallel Title: Internetausg. ---〉:Biomedical computing
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  • 4
    Journal/Serial
    Journal/Serial
    ¬The¬ journal of logic programming (from 1984-2000)
    New York, NY :North-Holland, ; 1.1984 - 46.2000
    Details
    Title: ¬The¬ journal of logic programming
    Publisher: New York, NY :North-Holland,
    Year of publication: 1984-2000
    Dates of Publication: 1.1984 - 46.2000
    ISSN: 0743-1066
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: Forts. ---〉:¬The¬ journal of logic and algebraic programming
    Parallel Title: Internetausg. ---〉:¬The¬ journal of logic and algebraic programming
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  • 5
    Book
    Book
    Computer personnel : a quarterly publ. of the Special Interest Group on Computer Personnel Research, SIGCPR (1971-1999)
    New York, NY :ACM, ; Nachgewiesen 2.1971 - 20.1999,4; damit Ersch. eingest.
    Details
    Title: Computer personnel : a quarterly publ. of the Special Interest Group on Computer Personnel Research, SIGCPR
    Publisher: New York, NY :ACM,
    Year of publication: 1971-1999
    Dates of Publication: Nachgewiesen 2.1971 - 20.1999,4; damit Ersch. eingest.
    ISSN: 0160-2497
    Type of Medium: Book
    Parallel Title: Internetausg. ---〉:Computer personnel
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  • 6
    Journal/Serial
    Journal/Serial
    CWI quarterly (from 1988-1999)
    Amsterdam :CWI, ; 1.1988 - 12.1999; damit Ersch. eingest.
    Details
    Title: CWI quarterly
    Author: Centrum voor Wiskunde en Informatica 〈Amsterdam〉
    Publisher: Amsterdam :CWI,
    Year of publication: 1988-1999
    Dates of Publication: 1.1988 - 12.1999; damit Ersch. eingest.
    ISSN: 0168-826X , 0922-5366
    Type of Medium: Journal/Serial
    Language: Undetermined
    Former Title: Vorg. ---〉:Centrum voor Wiskunde en Informatica 〈Amsterdam〉: CWI newsletter
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  • 7
    Journal/Serial
    Journal/Serial
    SIGART bulletin : a quarterly publ. of the Special Interest Group on Artificial Intelligence (from 1990-1998)
    New York, NY :ACM, ; 1.1990 - 9.1998
    Details
    Title: SIGART bulletin : a quarterly publ. of the Special Interest Group on Artificial Intelligence
    Author: Association for Computing Machinery / Special Interest Group on Artificial Intelligence
    Publisher: New York, NY :ACM,
    Year of publication: 1990-1998
    Dates of Publication: 1.1990 - 9.1998
    ISSN: 1053-4830
    Type of Medium: Journal/Serial
    Language: Undetermined
    Former Title: Vorg. ---〉:Association for Computing Machinery / Special Interest Group on Artificial Intelligence: SIGART newsletter
    Subsequent Title: Forts. ---〉:Intelligence
    Parallel Title: Internetausg. ---〉:Artificial intelligence
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  • 8
    Journal/Serial
    Journal/Serial
    Computers in physics / (from 1987-1998)
    Woodbury, NY :AIP, ; 1.1987,1(Nov./Dez.); 2.1988 - 12.1998
    Details
    Title: Computers in physics /
    Contributer: American Institute of Physics
    Publisher: Woodbury, NY :AIP,
    Year of publication: 1987-1998
    Dates of Publication: 1.1987,1(Nov./Dez.); 2.1988 - 12.1998
    ISSN: 0894-1866
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: Forts. ---〉:Computing in science & engineering
    URL: http://www.aip.org/cip/
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  • 9
    Journal/Serial
    Journal/Serial
    SIGNUM newsletter (from 1969-1998)
    New York, NY :ACM, ; 4.1969 - 33.1998,2; damit Ersch. eingest
    Details
    Title: SIGNUM newsletter
    Author: Association for Computing Machinery / Special Interest Group on Numerical Mathematics
    Publisher: New York, NY :ACM,
    Year of publication: 1969-1998
    Dates of Publication: 4.1969 - 33.1998,2; damit Ersch. eingest
    ISSN: 0163-5778
    Type of Medium: Journal/Serial
    Former Title: Vorg. ---〉:Association for Computing Machinery / Special Interest Committee on Numerical Mathematics: SICNUM newsletter
    Additional Information: 16,3=3,2 von:Association for Computing Machinery / Technical Committee on Fortran: FORTEC forum
    Parallel Title: Internetausg. ---〉:Numerical mathematics
    URL: Nur Table of Contents.
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  • 10
    Journal/Serial
    Journal/Serial
    Computer networks and ISDN systems : the international journal of computer and telecommunications networking (from 1985-1998)
    Amsterdam [u.a.] :Elsevier [u.a.], ; 9.1985 - 30.1998
    Details
    Title: Computer networks and ISDN systems : the international journal of computer and telecommunications networking
    Publisher: Amsterdam [u.a.] :Elsevier [u.a.],
    Year of publication: 1985-1998
    Dates of Publication: 9.1985 - 30.1998
    ISSN: 0169-7552 , 0376-5075
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: Vorg. u. Forts. ---〉:Computer networks
    Note: Computer networks for research in Europe
    Additional Information: In 14,1=15 von:Networkshop: Conference report
    Additional Information: 16,1/2=4; 17,4/5=5 von:European Networkshop: European Networkshop
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  • 11
    Journal/Serial
    Journal/Serial
    Unix review : the publication for the Unix community (from 1983-1998)
    San Francisco, Calif. :Miller Freeman, ; 1.1983 - 16.1998,3
    Details
    Title: Unix review : the publication for the Unix community
    Publisher: San Francisco, Calif. :Miller Freeman,
    Year of publication: 1983-1998
    Dates of Publication: 1.1983 - 16.1998,3
    ISSN: 0742-3136
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: Forts. ---〉:Unix review's performance computing
    Parallel Title: Internetausg. ---〉:Unix review.com
    URL: Zugriff lizenzfrei
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  • 12
    Journal/Serial
    Journal/Serial
    LISP and symbolic computation : an internat. journal ; a forum for current and envolving symbolic computing, focusing on LISP and object-oriented programming (from 1988-1997)
    Dordrecht [u.a.] :Kluwer Acad. Publ., ; 1.1988 - 10.1997
    Details
    Title: LISP and symbolic computation : an internat. journal ; a forum for current and envolving symbolic computing, focusing on LISP and object-oriented programming
    Publisher: Dordrecht [u.a.] :Kluwer Acad. Publ.,
    Year of publication: 1988-1997
    Dates of Publication: 1.1988 - 10.1997
    ISSN: 0892-4635
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: Forts. ---〉:Higher order and symbolic computation
    Parallel Title: Internetausg. ---〉:Higher-order and symbolic computation
    URL: Zugriff nur bis zu den Abstracts möglich.
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  • 13
    Journal/Serial
    Journal/Serial
    Supercomputer : bimonthly magazine on supercomputing in the Netherlands (from 1984-1997)
    Amsterdam :Amsterdam Universities Computing Centre, ; Nr. 1.1984 - 69.1997; damit Ersch. eingest.
    Details
    Title: Supercomputer : bimonthly magazine on supercomputing in the Netherlands
    Publisher: Amsterdam :Amsterdam Universities Computing Centre,
    Year of publication: 1984-1997
    Dates of Publication: Nr. 1.1984 - 69.1997; damit Ersch. eingest.
    ISSN: 0168-7875
    Type of Medium: Journal/Serial
    Language: Undetermined
    Note: Teils auch mit Jg.-Zählung
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  • 14
    Journal/Serial
    Journal/Serial
    ¬The¬ international journal of supercomputer applications and high performance computing (from 1987-1997)
    Thousand Oaks, Calif. :Sage Science Press, ; 1.1987 - 11.1997
    Details
    Title: ¬The¬ international journal of supercomputer applications and high performance computing
    Publisher: Thousand Oaks, Calif. :Sage Science Press,
    Year of publication: 1987-1997
    Dates of Publication: 1.1987 - 11.1997
    ISSN: 1078-3482 , 0890-2720
    Type of Medium: Journal/Serial
    Subsequent Title: Forts. ---〉:¬The¬ international journal of high performance computing applications
    Parallel Title: Internetausg. ---〉:¬The¬ international journal of high performance computing applications
    URL: Zugriff auf diese Zeitschrift für die Jahrgänge 3. 1989 - 11. 1997 innerhalb der ZIB Domain (IP Adressen: 130.73.*.*) möglich.
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  • 15
    Book
    Book
    Online : erfolgreiches Informationsmanagement, ADI-Nachrichten, ÖVD ; Organ d. ADI - Anwenderverband Deutscher Informationsverarbeiter e.V (1973-1997)
    Bergheim :DATACOM-Zeitschriften-Verl., | Köln Müller -1993,9 ; 11.1973 - 14.1976; 19.1981 - 20.1982; 1983 - 1994; 32.1995 - 34.1997,10
    Details
    Title: Online : erfolgreiches Informationsmanagement, ADI-Nachrichten, ÖVD ; Organ d. ADI - Anwenderverband Deutscher Informationsverarbeiter e.V
    Contributer: Anwenderverband Deutscher Informationsverarbeiter
    Publisher: Bergheim :DATACOM-Zeitschriften-Verl., , Köln Müller -1993,9
    Year of publication: 1973-1997
    Dates of Publication: 11.1973 - 14.1976; 19.1981 - 20.1982; 1983 - 1994; 32.1995 - 34.1997,10
    ISSN: 0340-1545 , 0179-6623 , 0342-9393
    Type of Medium: Book
    Language: Undetermined
    Former Title: Vorg. ---〉:Zeitschrift für Datenverarbeitung
    Subsequent Title: 15.1977 - 18.1980 ---〉:ADL-Verband für Informationsverarbeitung: ADL-Nachrichten, Online
    Subsequent Title: Aufgeg. in ---〉:Information week
    Note: Später ohne Zählung
    Additional Information: Beil. ---〉:Drucker spezial
    Additional Information: Beil. ---〉:Online / special
    Additional Information: Darin ---〉:Anwenderverband Deutscher Informationsverarbeiter: ADI-Nachrichten, ÖVD
    Additional Information: Beil. ---〉:Pro info
    Additional Information: Beil. ---〉:Online-Info
    Additional Information: 1996 darin ---〉:Datacom-Special
    Parallel Title: 19.1981 auch in ---〉:Öffentliche Verwaltung und Datenverarbeitung
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  • 16
    Journal/Serial
    Journal/Serial
    Unix mail : Europas erster Informationsdienst für Unix-Hersteller und -Anwender (from 1983-1996)
    München :Hanser, ; 1.1983 - 14.1996,6
    Details
    Title: Unix mail : Europas erster Informationsdienst für Unix-Hersteller und -Anwender
    Publisher: München :Hanser,
    Year of publication: 1983-1996
    Dates of Publication: 1.1983 - 14.1996,6
    ISSN: 0176-8654
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: Forts. ---〉:¬Die¬ blauen Blätter
    Parallel Title: CD-ROM-Ausg. ---〉:Unix mail, die blauen Blätter
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  • 17
    Journal/Serial
    Journal/Serial
    ¬The¬ X resource : a practical journal of the X window system (from 1991-1996)
    Sebastopol, Calif. :O'Reilly, ; 0.1991[Probeh.]; Nr. 1.1992 - 17.1996; damit Ersch. eingest.
    Details
    Title: ¬The¬ X resource : a practical journal of the X window system
    Publisher: Sebastopol, Calif. :O'Reilly,
    Year of publication: 1991-1996
    Dates of Publication: 0.1991[Probeh.]; Nr. 1.1992 - 17.1996; damit Ersch. eingest.
    ISSN: 1058-5591
    Type of Medium: Journal/Serial
    Language: Undetermined
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  • 18
    Journal/Serial
    Journal/Serial
    Cray channels : a Cray Research, Inc. publication (from 1984-1996)
    Minneapolis, Minn. :Cray Research, Inc., ; Nachgewiesen 6.1984 - 18.1996,2; damit Ersch. eingest.
    Details
    Title: Cray channels : a Cray Research, Inc. publication
    Contributer: Cray Research, Inc. 〈Mendota Heights, Minn.〉
    Publisher: Minneapolis, Minn. :Cray Research, Inc.,
    Year of publication: 1984-1996
    Dates of Publication: Nachgewiesen 6.1984 - 18.1996,2; damit Ersch. eingest.
    Type of Medium: Journal/Serial
    Language: Undetermined
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  • 19
    Journal/Serial
    Journal/Serial
    Nachrichtentechnische Zeitschrift : NTZ ; Zeitschrift für Informationstechnik u. Telekommunikation ; Organ der Nachrichtentechnischen Gesellschaft im VDE (from 1955-1995)
    Berlin :VDE-Verl., ; 8.1955,10 - 40.1987,2; 40.1987,6 - 48.1995,2
    Details
    Title: Nachrichtentechnische Zeitschrift : NTZ ; Zeitschrift für Informationstechnik u. Telekommunikation ; Organ der Nachrichtentechnischen Gesellschaft im VDE
    Contributer: Nachrichtentechnische Gesellschaft / Fachausschuß Informationsverarbeitung
    Publisher: Berlin :VDE-Verl.,
    Year of publication: 1955-1995
    Dates of Publication: 8.1955,10 - 40.1987,2; 40.1987,6 - 48.1995,2
    ISSN: 0027-707X
    Type of Medium: Journal/Serial
    Language: Undetermined
    Former Title: Vorg. ---〉:Fernmeldetechnische Zeitschrift
    Subsequent Title: 40.1987,3-5 u. Forts. ---〉:NTZ
    Note: Mikro-Elektronik
    Additional Information: Beih. ---〉:Nachrichtentechnische Fachberichte
    Additional Information: Index 1/10=11 von:Nachrichtentechnische Fachberichte
    Parallel Title: CD-ROM-Ausg. 1994 - 1995 ---〉:Elektronisches Zeitschriftenarchiv
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  • 20
    Journal/Serial
    Journal/Serial
    Zeitschrift für Operations-Research : ZOR ; mathematical methods of operations research (from 1972-1995)
    Heidelberg :Physica-Verl., ; 16.1972 - 42.1995
    Details
    Title: Zeitschrift für Operations-Research : ZOR ; mathematical methods of operations research
    Publisher: Heidelberg :Physica-Verl.,
    Year of publication: 1972-1995
    Dates of Publication: 16.1972 - 42.1995
    ISSN: 0340-9422
    Type of Medium: Journal/Serial
    Language: Undetermined
    Former Title: Vorg. ---〉:Ablauf- und Planungsforschung
    Subsequent Title: Forts. ---〉:Mathematical methods of operations research
    Note: Ser. A, Theorie = H. 1,3,5,7 d. Jg.; Ser. B, Praxis = H. 2,4,6,8 d. Jg. , Deutsche Gesellschaft für Operations-Research
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  • 21
    Journal/Serial
    Journal/Serial
    Annual review in automatic programming (from 1960-1995)
    Oxford [u.a.] :Pergamon Press, ; 1.1960 - 19.1995
    Details
    Title: Annual review in automatic programming
    Publisher: Oxford [u.a.] :Pergamon Press,
    Year of publication: 1960-1995
    Dates of Publication: 1.1960 - 19.1995
    ISSN: 0066-4138
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: Forts. ---〉:Annual reviews in control
    Additional Information: 1=3; 2=6, 3=11, 4=12; 5=13,2 von:International tracts in computer science and technology and their application
    Additional Information: 8=7; 9,2/3=8; 10=10; 11=11; 13,1=13; 14,1=15 von:Real time programming
    Additional Information: 12,1-12,2=2 von:Systems analysis and simulation
    Additional Information: 13,2=5 von:Control applications of nonlinear programming and optimization
    Parallel Title: Internetausg. ---〉:Annual reviews in control
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  • 22
    Journal/Serial
    Journal/Serial
    ORSA journal on computing / (from 1989-1995)
    Baltimore, Md., ; 1.1989 - 7.1995
    Details
    Title: ORSA journal on computing /
    Author: Operations Research Society of America
    Publisher: Baltimore, Md.,
    Year of publication: 1989-1995
    Dates of Publication: 1.1989 - 7.1995
    ISSN: 0899-1499
    Type of Medium: Journal/Serial
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  • 23
    Journal/Serial
    Journal/Serial
    IBM-Nachrichten / (from 1972-1995)
    Stuttgart :IBM, ; 22.1972,Apr. - 45.1995 = Nr. 210-323; damit Ersch. eingest.
    Details
    Title: IBM-Nachrichten /
    Author: IBM Deutschland GmbH 〈Stuttgart〉
    Publisher: Stuttgart :IBM,
    Year of publication: 1972-1995
    Dates of Publication: 22.1972,Apr. - 45.1995 = Nr. 210-323; damit Ersch. eingest.
    ISSN: 0018-8662
    Type of Medium: Journal/Serial
    Language: Undetermined
    Former Title: Vorg. ---〉:Internationale Büro-Maschinen-Gesellschaft Deutschland 〈Sindelfingen〉: IBM-Nachrichten
    Additional Information: Beil. ---〉:Hollerith-Mitteilungen
    Parallel Title: CD-ROM-Ausg. ---〉:IBM Deutschland GmbH 〈Stuttgart〉: IBM-Nachrichten
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  • 24
    Journal/Serial
    Journal/Serial
    LISP pointers / (from 1987-1995)
    New York, NY :ACM Inc., ; 1.1987/88 - 4.1990/91; 5.1992; 6.1992/93; 7.1994 - 8.1995,2; damit Ersch. eingest.
    Details
    Title: LISP pointers /
    Publisher: New York, NY :ACM Inc.,
    Year of publication: 1987-1995
    Dates of Publication: 1.1987/88 - 4.1990/91; 5.1992; 6.1992/93; 7.1994 - 8.1995,2; damit Ersch. eingest.
    ISSN: 1045-3563
    Type of Medium: Journal/Serial
    Note: Special Interest Group on Programming Languages (SIGPLAN)
    Parallel Title: Internetausg. ---〉:Association for Computing Machinery / Special Interest Group on Programming Languages: ACM SIGPLAN LISP pointers
    URL: Nur Tables of contents.
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  • 25
    Journal/Serial
    Journal/Serial
    SIGMICRO newsletter : a quarterly publ. of the Special Interest Group on Microprogramming (from 1971-1995)
    New York, NY :ACM, ; 2.1971/72 - 16.1985; 19.1988 - 26.1995; damit Ersch. eingest.
    Details
    Title: SIGMICRO newsletter : a quarterly publ. of the Special Interest Group on Microprogramming
    Author: Association for Computing Machinery / Special Interest Group on Microprogramming
    Publisher: New York, NY :ACM,
    Year of publication: 1971-1995
    Dates of Publication: 2.1971/72 - 16.1985; 19.1988 - 26.1995; damit Ersch. eingest.
    ISSN: 0163-5751 , 1050-916X
    Type of Medium: Journal/Serial
    Language: Undetermined
    Former Title: Vorg. ---〉:Association for Computing Machinery / Special Interest Committee on Microprocessing: SICMICRO newsletter
    Subsequent Title: 17.1986 - 18.1987 ---〉:Association for Computing Machinery / Special Interest Group on Microprogramming: SIGMICRO TCMICRO newsletter
    Additional Information: Beil. ---〉:Microprogramming bibliography
    Additional Information: 9,4=11; 12,4=14; 13,4=15 von:Micro
    Additional Information: 20,3=22 von:International Workshop on Microprogramming and Microarchitecture: Annual International Workshop on Microprogramming and Microarchitecture
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  • 26
    Book
    Book
    Data-base 〈New York,NY〉 : db ; a quarterly publication of the Special Interest Group on Business Information Technology of the Association for Computing Machinery (1971-1994)
    New York, NY, ; 3.1971 - 25.1994
    Details
    Title: Data-base 〈New York,NY〉 : db ; a quarterly publication of the Special Interest Group on Business Information Technology of the Association for Computing Machinery
    Contributer: Association for Computing Machinery / Special Interest Group on Business Data Processing , Association for Computing Machinery / Special Interest Group on Business Information Technology
    Publisher: New York, NY,
    Year of publication: 1971-1994
    Dates of Publication: 3.1971 - 25.1994
    ISSN: 0095-0033
    Type of Medium: Book
    Former Title: Vorg. ---〉 SIGBDP news-letter
    Subsequent Title: Forts. ---〉:¬The¬ data-base for advances in information systems
    Additional Information: Einzelne Bd. zugl. Bd. von:Association for Computing Machinery / Special Interest Group on Management of Data: SIGMOD record
    Additional Information: 12,4u.13,1=2 von:Data-base directions
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  • 27
    Journal/Serial
    Journal/Serial
    MC 〈München〉 : Computerpraxis für technische Anwender (from 1981-1994)
    München :Franzis-Verl., ; 1981 - 1994,6
    Details
    Title: MC 〈München〉 : Computerpraxis für technische Anwender
    Publisher: München :Franzis-Verl.,
    Year of publication: 1981-1994
    Dates of Publication: 1981 - 1994,6
    ISSN: 0720-4442 , 0941-777X , 0943-5409
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: Aufgeg. in ---〉:DOS international
    Note: Auch mit fehlerhafter Jg.-Zählung im Impressum
    Additional Information: 1992 Sonderh. ---〉:WINbox
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  • 28
    Journal/Serial
    Journal/Serial
    SIGSMALL - PC notes : a publication of the Special Interest Group on Small and Personal Computing Systems and Applications, Association for Computing Machinery (from 1984-1993)
    New York, NY :ACM, ; 10.1984,4 - 19.1993/94,2(1993)
    Details
    Title: SIGSMALL - PC notes : a publication of the Special Interest Group on Small and Personal Computing Systems and Applications, Association for Computing Machinery
    Author: Association for Computing Machinery / Special Interest Group on Small and Personal Computing Systems and Applications
    Publisher: New York, NY :ACM,
    Year of publication: 1984-1993
    Dates of Publication: 10.1984,4 - 19.1993/94,2(1993)
    ISSN: 0893-2875
    Type of Medium: Journal/Serial
    Language: Undetermined
    Former Title: Vorg. ---〉:Association for Computing Machinery / Special Interest Group on Small Computing Systems and Applications: SIGSMALL newsletter
    Subsequent Title: Forts. ---〉:Association for Computing Machinery / Special Interest Group on Individual Computing Environments: SIGICE bulletin
    Note: Zählung von "SIGSMALL newsletter" übernommen
    Parallel Title: Internetausg. ---〉:Association for Computing Machinery / Special Interest Group on Small and Personal Computing Systems and Applications: ACM SIGSMALL - PC notes
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  • 29
    Journal/Serial
    Journal/Serial
    Impact of computing in science and engineering (from 1989-1993)
    Duluth, Minn. [u.a.], ; 1.1989 - 5.1993; damit Ersch. eingest.
    Details
    Title: Impact of computing in science and engineering
    Publisher: Duluth, Minn. [u.a.],
    Year of publication: 1989-1993
    Dates of Publication: 1.1989 - 5.1993; damit Ersch. eingest.
    ISSN: 0899-8248
    Type of Medium: Journal/Serial
    Language: Undetermined
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  • 30
    Journal/Serial
    Journal/Serial
    International journal of man machine studies (from 1969-1993)
    London [u.a.], ; 1.1969 - 39.1993
    Details
    Title: International journal of man machine studies
    Publisher: London [u.a.],
    Year of publication: 1969-1993
    Dates of Publication: 1.1969 - 39.1993
    ISSN: 0020-7373
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: Forts. ---〉:International journal of human - computer studies
    Note: Index 1/4.1969/72 in: 4.1972
    Additional Information: 10,3=5 von:Man Computer Communications Conference: Proceedings
    Parallel Title: Internetausg. ---〉:International journal of man machine studies
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  • 31
    Electronic Resource
    Electronic Resource
    Distribution of Free Methylarginines in Rat Tissues and in the Bovine Brain (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: A sensitive and specific method for determining three forms of methylarginine, i.e., NG-monomethylarginine, NG,NG-dimethylarginine, and NG,NG-dimethylarginine, in mammalian tissues was developed. After partial purification by ion-exchange chromatography, the methyl-arginines were derivatized to phenylthiocarbamyl compounds and quantitatively determined using HPLC with a reverse-phase C18 column. In rat organs, the highest concentrations of methylarginines were observed in the spleen. In rat brain, cerebellum and olfactory bulb contained large amounts of NG-monomethylarginine and NG,NG-dimethylarginine. A detailed study of the distribution of methylarginines in the bovine brain was also made, and the concentration of NG,NG-dimethylarginine was almost the same in all regions. The cerebellar gray matter, hippocampus, and hypothalamus contained large amounts of methylarginines. The distribution of methylarginines seems to parallel the distribution of nitric oxide synthase, which is known to be inhibited by NG-monomethylarginine. This may indicate that methylarginines play some role in controlling nitric oxide synthase activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10088.x
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  • 32
    Electronic Resource
    Electronic Resource
    Stimulation of Cultured Cerebellar Granule Cells via Glutamate Receptors Induces TRE- and CRE-Binding Activities Mediated by Common DNA-Binding Complexes (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: By use of nuclear mini-extracts prepared from cultured cerebellar granule cells in a gel-mobility assay, exogenous N-methyl-D-aspartate (NMDA) or kainate was shown to increase both 12-O-tetradecanoylphorbol 13-acetate-responsive element (TRE)- and cyclic AMP-responsive element (CRE)-binding activity. These increases were specifically prevented by the NMDA receptor antagonist D,L-2-amino-5-phosphonovalerate and the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione, respectively. The increase of TRE-binding activity was dependent on de novo protein synthesis, and its inductions by both NMDA and kainate required extracellular Ca2+. TRE-binding activity was competitively inhibited by the CRE, and vice versa, showing higher DNA-binding affinity to the CRE than to the TRE. A proteolytic clipping bandshift assay demonstrated that the increase in CRE-binding activity could be mediated by the TRE-binding activity. Thus, the TRE-binding activity cross-binding to the CRE could be activated by NMDA or kainate stimulation. The involvement of c-Fos or Fos-related proteins in the TRE- and CRE-binding complexes was shown by a supershift gel-mobility assay using anti-c-Fos antiserum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10096.x
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  • 33
    Electronic Resource
    Electronic Resource
    Quantification of Rat Cerebral Cortex Na+,K+-ATPase: Effect of Age and Potassium Depletion (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Na+,K+-ATPase concentration in rat cerebral cortex was studied by vanadate-facilitated [3H]ouabain binding to intact samples and by K+-dependent 3-O-methylfluorescein phosphatase activity determinations in crude homogenates. Methodological errors of both methods were evaluated. [3H]Ouabain binding to cerebral cortex obtained from 12-week-old rats measured incubating samples in buffer containing [3H]ouabain, and ouabain at a final concentration of 1 × 10–6 mol/L gave a value of 11,351 ± 177 (n = 5) pmol/g wet weight (mean ± SEM) without any significant variation between the lobes. Evaluation of affinity for ouabain was in agreement with a heterogeneous population of [3H]ouabain binding sites. K+-dependent 3-O-methylfluorescein phosphatase activity in crude cerebral homogenates of age-matched rats was 7.24 ± 0.14 (n = 5) μmol/min/g wet weight, corresponding to a Na+,K+-ATPase concentration of 12,209 ± 236 pmol/g wet weight. It was concluded that the present methods were suitable for quantitative studies of cerebral cortex Na+,K+-ATPase. The concentration of rat cerebral cortex Na+,K+-ATPase showed ∼10-fold increase within the first 4 weeks of life to reach a plateau of ∼11,000–12,000 pmol/g wet weight, indicating a larger synthesis of Na+,K+ pumps than tissue mass in rat cerebral cortex during the first 4 weeks of development. K+ depletion induced by K+-deficient fodder for 2 weeks resulted in a slight tendency toward a reduction in K+ content (6%, p 〉 0.5) and Na+,K+-ATPase concentration (3%, p 〉 0.4) in cerebral cortex, whereas soleus muscle K+ content and Na+,K+-ATPase concentration were decreased by 30 (p 〈 0.02) and 32% (p 〈 0.001), respectively. Hence, during K+ depletion, cerebral cortex can maintain almost normal K+ homeostasis, whereas K+ as well as Na+,K+ pumps are lost from skeletal muscles.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10100.x
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  • 34
    Electronic Resource
    Electronic Resource
    Nicotinic Agonists, Phorbol Esters, and Growth Factors Activate Two Extracellular Signal-Regulated Kinases, ERK1 and ERK2, in Bovine Chromaffin Cells (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Treatment of bovine chromaffin cells with nicotinic agonists, phorbol esters, and growth factors increases protein kinase activity toward microtubule-associated protein-2 and myelin basic protein (MBP) in vitro. To characterize the kinases that are activated by these agents, we separated chromaffin cell proteins by electrophoresis in sodium dodecyl sulfate-polyacrylamide gels into which MBP had been incorporated, allowed the proteins to renature, and then assayed MBP kinase activity by incubating the gels with [γ-32P]ATP. Chromaffin cells contain a family of kinases that phosphorylate MBP in vitro. Two of these kinases, of Mr 46,000 and 42,000 (PK46 and PK42), were activated by treatment of the cells with dimethylphenylpiperazinium (DMPP), phorbol 12,13-dibutyrate (PDBu), or insulin-like growth factor I (IGF-I). Activation of PK46 and PK42 by DMPP was dependent on extracellular Ca2+, whereas the effects of PDBu and IGF-I were Ca2+ independent. Down-regulation of protein kinase C by incubation of the cells with PDBu abolished the activation of PK46 and PK42 by DMPP, PDBu, and IGF-I. Staurosporine, a protein kinase C inhibitor, prevented the activation of PK46 and PK42 by DMPP and PDBu but did not block the activation of these kinases by IGF-I. Immunoblotting experiments with antiphosphotyrosine (anti-PTyr) antibodies demonstrated that agents that increased the kinase activities of PK46 and PK42 also increased the apparent PTyr content of Mr 46,000 and 42,000 proteins. PK46 and PK42 comigrated with proteins that reacted with antibodies against extracellular signal-regulated kinases (ERKs). Thus, PK46 and PK42 appear to be the bovine homologues of ERK1 and ERK2. These kinases are regulated by multiple pathways and may play a role in the mechanism by which a variety of agonists regulate chromaffin cell function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10104.x
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  • 35
    Electronic Resource
    Electronic Resource
    Recovery of Cholinergic Phenotype in the Injured Rat Neostriatum: Roles for Endogenous and Exogenous Nerve Growth Factor (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Polyclonal antibodies against recombinant human nerve growth factor (rhNGF) potently inhibited PC12 neurite outgrowth, blocked high-affinity 125I-rhNGF binding but not its receptor, and cross-reacted with rat, mouse, and human nerve growth factor (NGF) but not with brain-derived neurotrophic factor, neurotrophin-3, ciliary neurotrophic factor, insulin-like growth factor, epidermal growth factor, or activin A. Immunocytochemistry revealed many NGF-positive neurons in the rat neostriatum. The NGF-positive neurons disappeared by 3 days after mechanical injury to the neostriatum and were replaced by intensely NGF- and glial fibrillary acidic protein-positive astrocytes. Enzyme-linked immunosorbent assay measurements revealed that the NGF content of the injured striatum was elevated by eightfold 3 days postinjury and by twofold 2 weeks later. The high-affinity choline uptake (HACU) into cholinergic nerve terminals was decreased by 23% at 2 and 4 weeks postinjury, yet choline acetyltransferase (ChAT) activity in these neurons was unchanged at 2 weeks and decreased by 14% at 4 weeks. Daily infusion of 1 μg of rhNGF into the injury area did not alter the loss of HACU. However, this treatment elevated ChAT activity by 23–29% above intact neostriatal levels and by 53–65% relative to HACU at both survival times. Thus, lesion-induced increases in NGF levels within astrocytes are associated with maintenance of striatal ChAT activity at normal levels following cholinergic injury, even with decreases in HACU. Pharmacologic doses of rhNGF can further augment ChAT activity in damaged cholinergic neurons, showing the usefulness of exogenous NGF even when endogenous NGF is elevated in response to injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10108.x
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  • 36
    Electronic Resource
    Electronic Resource
    Carboxypeptidase M in Brain and Peripheral Nerves (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Carboxypeptidase M (CPM), a plasma membrane-bound enzyme, cleaves C-terminal basic amino acids with a neutral pH optimum. We studied its distribution in human, baboon, and dog brain and in dog peripheral nerves. Areas were dissected, homogenized, centrifuged, and assayed for activity with dansyl-Ala-Arg. The corpus callosum and the pyramidal and optic tract were especially rich in CPM, whereas basal ganglia and cortex had low activity. The identity of the basic carboxypeptidase activity with CPM was shown by similarities in subcellular localization, membrane attachment, substrate hydrolysis, inhibition by a specific basic carboxypeptidase inhibitor, and cross-reaction with anti-human CPM antiserum. This antiserum immunoprecipitated an average of 85% of the activity in human and baboon brain and ∼66% in dog brain. CPM copurified with myelin extracted from the brain. Consistent with results obtained in placenta and cultured kidney cells, CPM in the brain appears to be membrane-bound via a phosphatidylinositol glycan anchor. In the peripheral nerves, the specific activity in dog sciatic nerve and in vagus was high (98 and 149 nmol/h/mg of protein, respectively). In immunohistochemical studies, glia in the brain, which appear to be oligodendrocytes or astrocytes, and the outer aspects of myelin sheaths and Schwann cells in sciatic and vagus nerves were stained. We conclude that in some areas of the CNS and the PNS, CPM is closely associated with myelin and myelin-forming cells. Northern blot analysis revealed the presence of mRNA coding for CPM in the brain, showing that the enzyme is indeed synthesized there.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10112.x
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  • 37
    Electronic Resource
    Electronic Resource
    Cytosolic Free Calcium and Gene Expression During Chemical Hypoxia (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Understanding the cellular response to hypoxia may help elucidate the role of altered oxidation in neuronal death or abnormal cell function. In PC 12 cells, 30 min of chemical hypoxia (i.e., KCN) reduced ATP concentrations by 92%, but diminished viability by only 10%. Ten minutes of hypoxia increased cytosolic free calcium ([Ca2+]i) 2.5-fold above control, but after 30 min of hypoxia, [Ca2+]i was slightly below that of nonhypoxic cells. Short periods of hypoxia also exaggerated the K+-induced elevation of [Ca2+]i, but by 30 min these ATP-depleted cells reestablished a calcium gradient that was equal to nonhypoxic, K+-depolarized cells. Thus, 30 min of severe ATP depletion left [Ca2+]i and viability relatively unaffected. Nerve growth factor caused slight, but significant, improvements in ATP and viability of hypoxic cells, but had no effect on [Ca2+]i. Although [Ca2+]i was equivalent in control and hypoxic cells after 30 or 60 min, hypoxia abolished the K+-stimulated elevation of [Ca2+]i. The nerve growth factor induction of c-fos, an indicator of the genomic response, was diminished by sim 80%. Thus, hypoxic PC 12 cells with greatly reduced ATP stores maintained normal [Ca2+]i, but their ability to respond to external stimulation was impaired. Further, the reduced oxidation that occurs in the brain in a variety of pathological conditions may interfere with the cellular response to stimulation and growth factors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11017.x
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  • 38
    Electronic Resource
    Electronic Resource
    Relationship Between Plasma and Brain Large Neutral Amino Acids in Rats Fed Diets with Different Compositions at Different Times of the Day (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Large neutral amino acids (LNAAs) compete with each other for carrier-mediated transport through the blood-brain barrier into the brain. The relative plasma concentration, expressed as the ratio of each LNAA to the sum of LNAAs, is considered the main regulator of brain LNAA concentrations. In order to investigate the consistency of this assumption throughout a 24-h period, we have compared the relationship of plasma LNAAs to brain LNAAs among groups of rats fed diets containing various amounts of protein (in order to obtain a wide range of plasma LNAA levels) at two different phases of the light/dark cycle (0900 and 2100 hours). The relationship between plasma and brain LNAAs was found to be dependent on both diet and the time of day. Similar plasma amino acid concentrations in the morning and in the evening contrasted with different brain concentrations. Furthermore, previous findings that brain LNAA concentrations are influenced by plasma amino acid concentrations were confirmed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11022.x
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  • 39
    Electronic Resource
    Electronic Resource
    3-[(±)-2-Carboxypiperazin-4-yl]propyl-1-Phosphonic Acid Recognizes Two N-Methyl-D-Aspartate Binding Sites in Rat Cerebral Cortex Membranes (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Binding of 3-[(pmn)-2-carboxypiperazin-4-yl][3H]-propyl-1-phosphonic acid ([3H]CPP), a competitive inhibitor of N-methyl-D-aspartate (NMDA), has been studied in synaptic plasma membranes from rat cerebral cortex. Computer analysis of saturation and homologous displacement isotherms deriving from these plasma membranes indicated the existence of two binding sites: a specific, saturable, high-affinity binding site with a pKD value of 7.53 pmn 0.03 (29.5 nM) and a maximum binding value (Bmax) of 2.25 pmn 0.36 pmol/mg of protein, and a low-affinity site with a KD of approximately 600 nM and a Bmax of 7.0 pmol/mg of protein. It is argued that, in the light of current literature evidence, the low-affinity binding site may represent an agonist-dependent receptor, linked to physiological processes such as neurotransmitter release and channel regulation, whereas the high-affinity binding site may be linked to an antagonist-preferred receptor, for which no function has yet been reported.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11019.x
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  • 40
    Electronic Resource
    Electronic Resource
    Regional Effects of Sodium Valproate on Extracellular Concentrations of 5-Hydroxytryptamine, Dopamine, and Their Metabolites in the Rat Brain: An In Vivo Microdialysis Study (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effects of sodium valproate (VPA; 100, 200, and 400 mg/kg, i.p.) on ventral hippocampal and anterior caudate putamen extracellular levels ofdopamine (DA) and 5-hydroxytryptamine (5-HT) were examined using in vivo microdialysis. VPA induced dose-related increases in dialysate DA, 3,4-dihydroxyphenylacetic acid, and 5-HT in the ventral hippocampus. Anterior caudate putamen dialysate 5-HT was also dose dependently elevated by the drug, whereas DA levels tended to decrease with increasing VPA dose. In contrast, VPA (200, 400, and 800 mg/kg, i.p.) produced no significant elevation of DA in posterior caudate putamen dialysates, although 5-HT levels were significantly elevated at the 400- and 800-mg/kg doses. In all three regions studied, dialysate concentrations of 5-hydroxyindoleacetic acid and homovanillic acid remained at basal levels following VPA treatments. The results are discussed with regard to the possible anticonvulsant mode of action of VPA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11001.x
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  • 41
    Electronic Resource
    Electronic Resource
    Brief Instructions to Authors (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11040.x
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  • 42
    Electronic Resource
    Electronic Resource
    Rat Brain Creatine Kinase Messenger RNA Levels Are High in Primary Cultures of Brain Astrocytes and Oligodendrocytes and Low in Neurons (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Rat brain creatine kinase (CKB) gene expression is highest in the brain but is also detectable at lower levels in some other tissues. In the brain, the CKB enzyme is thought to be involved in the regeneration of ATP necessary for transport of ions and neurotransmitters. To understand the molecular events that lead to high CKB expression in the brain, we have determined the steady-state levels of CKB mRNA in homogeneous cultures of primary rat brain astrocytes, oligodendrocytes, and neurons. Northern blot analysis showed that whereas the 1.4-kb CKB mRNA was detectable in neurons, the level was about 17-fold higher in oligodendrocytes and 15-fold higher in astrocytes. The blots were hybridized with a CKB-specific 32P-antisense RNA probe, complementary to the 3’untranslated sequence of CKB, which hybridizes to CKB mRNA but not CKM mRNA. Also, the 5’and 3’ends of CKB mRNA from the glial cells were mapped, using exon-specific antisense probes in the RNase-protection assay, and were found to be the same in astrocytes and oligodendrocytes. This indicated that (a) the site of in vivo transcription initiation in astrocytes and oligodendrocytes was directed exclusively by the downstream, nonconcensus TTAA sequence at -25 bp in the CKB promoter that is also utilized by all other cell types that express CKB and (b) the 3’end of mature CKB mRNA was the same in astrocytes and oligodendrocytes. In addition, there was no detectable alternate splicing in exon 1, 2, or 8 of CKB mRNA in rat astrocytes and oligodendrocytes. Also, our studies showed that 1.4-kb CKB mRNA is expressed in established C6 glioma cells at an intermediate level about threefold higher than that in primary neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11028.x
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  • 43
    Electronic Resource
    Electronic Resource
    Tyrosine Phosphorylation of Microtubule-Associated Protein Kinase After Transient Ischemia in the Gerbil Brain (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The tyrosine phosphorylation of microtubule-associated protein (MAP) kinase was examined in the gerbil brain after transient ischemia and reperfusion. Phosphorylation of MAP kinase was maximal within 1 min of reperfusion following 5 min of ischemia and returned to control levels as early as 5 min postischemia. The greatest increase in MAP kinase phosphorylation was detected in the hippocampus, with minor increases in other ischemic regions of the brain. Several tyrosine-phosphorylated proteins were detected in the gerbil hippocampus; however, the ischemia and reperfusion injury only increased tyrosine phosphorylation of MAP kinase. The increase in tyrosine phosphorylation was prevented by the N-methyl-D-aspartate (NMDA) receptor blocker (+)-MK-801, whereas a non-NMDA receptor blocker, 6-cyano-7-nitroquinoxaline-2,3-dione, was ineffective. Pretreatment of gerbils with calcium channel blockers also prevented the tyrosine phosphorylation of MAP kinase in the ischemic brain. Altogether, these results imply an involvement of glutamate receptors and calcium during the tyrosine phosphorylation of MAP kinase. Tyrosine phosphorylation was also prevented when ischemia and reperfusion were conducted under hypothermic conditions, which protect against neurodegenerative damage. These findings implicate a role for MAP kinase in neuronal damage resulting from ischemia and reperfusion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11032.x
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  • 44
    Electronic Resource
    Electronic Resource
    Okadaic Acid, a Protein Phosphatase Inhibitor, Inhibits Nerve Growth Factor-Directed Neurite Outgrowth in PC 12 Cells (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The biochemical mechanisms involved in neurite outgrowth in response to nerve growth factor (NGF) have yet to be completely resolved. Several recent studies have demonstrated that protein kinase activity plays a critical role in neurite outgrowth. However, little information exists about the role of protein phosphatases in the process. In the present study, okadaic acid, a phosphatase inhibitor (specific for types 2A and 1) and tumor promoter, was used to investigate the role of protein phosphatases in neurite outgrowth in PC12 cells. PC12 cells cultured in the presence of 50 ng/ml of NGF started to extend neurites after 1 day. After 3 days, 20–25% of the cells had neurites. Okadaic acid inhibited the rate of neurite outgrowth elicited by NGF with an IC50, of sim7 nM. This inhibition was rapidly reversed after washout of okadaic acid. Okadaic acid also enhanced the neurite degeneration of NGF-primed PC12 cells, indicating that continual phosphatase activity is required to maintain neurites. Taken together, these results reveal the presence of an okadaic acid-sensitive pathway in neurite outgrowth and imply that protein phosphatase plays a positive role in regulating the neuritogenic effects of NGF.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11034.x
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  • 45
    Electronic Resource
    Electronic Resource
    Calendar of Events (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11041.x
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  • 46
    Electronic Resource
    Electronic Resource
    Two Pathways of Cyclic GMP Production Through Glutamate Receptor-Mediated Nitric Oxide Synthesis (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The selective agonists for the metabotropic glutamate receptor and the ionotropic non-Ar-methyl-D-aspar-tate (NMDA) glutamate receptor, (±)-l-aminocyclopen-tane-/ra/w-l,3-dicarboxylic acid (ACPD) and (R,S)-α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA), respectively, increased the cyclic GMP (cGMP) content in cerebellar slices prepared from adult rats. The ACPD-induced rise in cGMP level was blocked by compounds known to antagonize metabotropic glutamate receptors, such as DL-2-amino-3-phosphonopropionic acid and L-2-amino-4-phosphonobutyric acid, but not by ionotropic glutamate receptor antagonists, D-2-amino-5-phosphonovale-ric acid and 6 - cyano - 7 - nitroquinoxaline -2,3– dione (CNQX), whereas the AMPA-induced rise in cGMP level was suppressed by CNQX. Both rises in cGMP level involved nitric oxide synthase (NOS), because NG-methyl-L-arginine (NMLA), an inhibitor of NOS, blocked both cGMP level rises, and excess L-arginine reversed the effect of NMLA. After lithium chloride treatment, which could exhaust phosphatidylinositol phosphates, ACPD no longer increased cGMP levels, whereas AMPA was still effective. In a calcium-free medium, ACPD still induced a rise in cGMP level, whereas AMPA did not. When the molecular layer was isolated to determine the cGMP content separately from that in the rest of the cerebellar cortex, it was found that ACPD raised the cGMP level mainly in the molecular layer, whereas AMPA raised it in both sections. These results suggest that ACPD enhances the cGMP level through activation of NOS independently of extracellular calcium, most likely by calcium release from intracellular stores triggered by metabotropic glutamate receptors linked to phosphoinositide breakdown, whereas AMPA activates the enzyme by calcium entry from the extracellular space triggered by ionotropic non-NMDA glutamate receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08429.x
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  • 47
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    Analogues of Somatostatin Bind Selectively to Brain Somatostatin Receptor Subtypes (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Somatostatin (SRIF) is a neurotransmitter that produces its multiple effects in the CNS through interactions with membrane-bound receptors. Subtypes of SRIF receptors are found in the CNS that are distinguished by their sensitivities to the cyclic hexapeptide MK-678, such that SRIF, receptors are sensitive to MK-678 and SRIF2 receptors are insensitive to MK-678. In the present study, we further examined the selectivities of a series of structurally diverse SRIF analogues for SRIF receptor subtypes. SRIF receptors were labeled by 125I-Tyr11 SRIF, which has indistinguishable affinities for SRIF receptor subtypes. The inhibition by MK-678 was incomplete, indicating this peptide is highly selective for a subtype of SRIF receptor that we have termed the SRIF, receptor. The binding of 125I-MK-678 to SRIF, receptors was monophasically inhibited by SRIF, the octapeptides (such as SMS-201–995), and the hexapeptides (such as MK-678), consistent with the highly selective labeling of a subtype of SRIF receptor. In contrast, the smaller CGP-23996-like analogues did not inhibit 125I-MK-678 binding to SRIF, receptors. The binding of 125I-CGP-23996 to SRIF receptors was inhibited by SRIF and the octapeptides with Hill coefficients of 〈 1, indicating that 128I-CGP-23996 labels multiple SRIF receptor subtypes. The hexapeptides and CGP-23996-like compounds produced only partial inhibitions of 125I-CGP-23996 binding, which were additive, indicating selective interactions of these compounds with the different receptor subpopulations labeled by 125I-CGP-23996. 125I-Tyr11-SRIF binding and 125I-CGP-23996 binding to SRIF receptors were likewise only partially affected by 100 μM guanosine 5′-O-(3-thiotriphosphate) (GTPγS), a concentration that completely abolishes specific 125I-MK-678 binding to SRIF, receptors. The component of 125I-CGP-23996 labeling that was sensitive to GTPγS was also MK-678 sensitive. Thus, two subpopulations of SRIF receptors exist in the CNS. The SRIF, receptor is sensitive to cyclic hexapeptides such as MK-678 and to GTPγS but insensitive to smaller CGP-23996-like compounds. The SRIF2 receptor is sensitive to the CGP-23996-like compounds and can be selectively labeled by 125I-CGP-23996 in the presence of high concentrations of the hexapeptides or GTPγS because, unlike the SRIF, receptor, the SRIF2 receptor is insensitive to these agents. The SRIF receptor subtype-selective peptide analogues will be useful in the future characterization of the functions mediated by SRIF receptor subtypes in the CNS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08433.x
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  • 48
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    Global Forebrain Ischemia Induces a Posttranslational Modification of Multifunctional Calcium- and Calmodulin-Dependent Kinase II (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The activity of multifunctional calcium/calmodulin-dependent protein kinase II (CaM kinase II) has recently been shown to be inhibited by transient global ischemia. To investigate the nature of ischemia-induced inhibition of the enzyme, CaM kinase II was purified to 〉 1,000-fold from brains of control and ischemic gerbils. The characteristics of CaM kinase II from control and ischemic preparations were compared by numerous parameters. Kinetic analysis of purified control and ischemic CaM kinase II was performed for autophosphorylation properties, ATP, magnesium, calcium, and calmodulin affinity, immunoreactivity, and substrate recognition. Ischemia induced a reproducible inhibition of CaM kinase II activity, which could not be overcome by increasing the concentration of any of the reaction parameters. Ischemic CaM kinase II was not different from control enzyme in affinity for calmodulin, Ca2+, Mg2+, or exogenously added substrate or rate of autophosphorylation. CaM kinase II isolated from ischemic gerbils displayed decreased immunoreactivity with a monoclonal antibody (immunoglobulin G3) directed toward the β subunit of the enzyme. In addition, ischemia caused a significant decrease in affinity of CaM kinase II for ATP when measured by extent of autophosphorylation. To characterize further the decrease in ATP affinity of CaM kinase II, the covalent-binding ATP analog 8-azidoadenosine-5′-[α-32P]triphosphate was used. Covalent binding of 25 μM azido-ATP was decreased 40.4 ± 12.3% in ischemic CaM kinase II when compared with control enzyme (n = 5; p 〈 0.01 by paired Student's t test). Thus, CaM kinase II levels for ischemia and control fractions were equivalent by protein staining, percent recovery, and calmodulin binding but were significantly different by immunoreactivity and ATP binding. The data are consistent with the hypothesis that ischemia induces a posttranslational modification that alters ATP binding in CaM kinase II and that results in an apparent decrease in enzymatic activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08431.x
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  • 49
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    Effect of N,N-Dicyclohexylcarbodiimide on Acetylcholine Release from Torpedo Synaptosomes and Proteoliposomes Reconstituted with the Proteolipid Mediatophore (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The mediatophore is a presynaptic membrane protein that has been shown to translocate acetylcholine (ACh) under calcium stimulation when reconstituted into artificial membranes. The mediatophore subunit, a 15-kDa proteolipid, presents a very high sequence homology with the N,N′-dicyclohexylcarbodiimide (DCCD)-binding proteolipid subunit of the vacuolar-type H+-ATPase. This prompted us to study the effect of DCCD, a potent blocker of proton translocation, on calcium-dependent ACh release. The present work shows that DCCD has no effect on ACh translocation either from Torpedo synaptosomes or from proteoliposomes reconstituted with purified mediatophore. However, using [14C]DCCD, we were able to demonstrate that the drug does bind to the 15-kDa proteolipid subunit of the mediatophore. These results suggest that although the 15-kDa proteolipid subunits of the mediatophore and the vacuolar H+-ATPase may be identical, different domains of these proteins are involved in proton translocation and calcium-dependent ACh release and that the two proteins have a different membrane organization.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08437.x
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  • 50
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    Characterization of the Irreversible Inhibition of High-Affinity Choline Transport Produced by Hemicholinium Mustard (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The inhibition of high-affinity choline transport by hemicholinium mustard (HCM), an alkylating analogue of hemicholinium-3, was examined in rat brain synaptosomes and guinea pig myenteric plexus. In synaptosomes, 50% high-affinity choline transport inhibition occurs with an HCM concentration of 104 nM (4-min incubation). A 10-min preincubation with 10 nM HCM results in essentially complete (〉95%) inactivation that persists after washing. Low-affinity choline transport in synaptosomes is unaffected by HCM inhibition at all concentrations examined (1–50 μM). Time course experiments indicate that the maximum irreversible inhibition (58%) seen after a 1-min preincubation with 500 nM HCM decreases to 46% inhibition after a 15-min preincubation; however, analysis of variance reveals that this difference is not significant. HCM inhibition of acetylcholine release from myenteric plexus-longitudinal muscle preparations persists for at least 2 h after removal of drug from the incubation bath; this inactivation can be prevented by coincubation with a high choline concentration during treatment with the mustard. In contrast, inhibition produced by the parent compound hemicholinium-3 is largely reversed by washing in both preparations: examined. The observed potency and selectivity of HCM suggest its usefulness as a covalent probe for high-affinity choline transport.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08441.x
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  • 51
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    Lesion-Induced Changes in the Production of Newly Synthesized and Secreted Apo-E and Other Molecules Are Independent of the Concomitant Recruitment of Blood-Borne Macrophages into Injured Peripheral Nerves (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Peripheral nerve injury produces Wallerian degeneration characterized by a change in the composition of resident nonneuronal cells: macrophages are recruited from the circulation to join Schwann, fibroblast, and endothelial cells. At the same time, the nonneuronal cell population exhibits, as a whole, alterations in synthesis and secretion of diffusible molecules, some of which are instrumental in nerve repair mechanisms. In this study, we determined whether changes in the production of secreted molecules depend on the concomitant modification in cell composition. Therefore, we studied the secretion of newly synthesized molecules by defined cell populations of intact nerves, intact nerve explants undergoing in vitro axonal degeneration, in vivo degenerating nerves, and recruited cells. Nerves were incubated in serum-free, [35S]methionine-containing media. Secreted, radioactively labeled proteins were precipitated from the medium and analyzed by gel electrophoresis. Reduced production of 43-, 46-, and 48-kDa proteins and increased production of 33–34-, 37-, 49-, 59–, and 67-kDa proteins were detected in in situ degenerating nerves. High-density ultracentrifugation and immunoblot analysis revealed that the 33–34-kDa protein is apolipoprotein-E (apo-E). Similar alterations in the production of these molecules were detected in intact nerve explants from which blood-borne cells were excluded. Apo-E, 37-, 49-, 59-, and 67-kDa proteins were also produced in frozen nerves that lacked the intact nerve nonneuronal cell population. Instead, these preparations contained blood-borne cells, primarily macrophages. Thus, change in the production of a substantial number of secreted molecules, apo-E included, is a characteristic response to axonal disintegration of the nonneuronal cells resident in intact nerves. Recruited macrophages, although not required, contribute to the production of apo-E and other secreted molecules. The production of apo-E and 45-kDa proteins was inhibited, and that of 37-kDa proteins increased in the presence of NH4Cl, further suggesting that lysosomal activity plays a role in the regulation of the production of these molecules.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08439.x
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  • 52
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    Characterization of the 5-Hydroxytryptamine Receptor Modulating the Release of 5-[3H]Hydroxytryptamine in Slices of the Human Neocortex (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In the rat brain, the presynaptic 5-hydroxytrypt-amine (5-HT) autoreceptors located on 5-HT terminals correspond to the 5-HT1B subtype. The presence of a 5-HT receptor probably located on 5-HT nerve endings and modulating transmitter release in the human neocortex has been reported, but its detailed pharmacological characterization is not yet available. On the other hand, receptor binding and autoradiographic results indicate that the 5-HT1B receptor subtype is not present in the human brain. We, therefore, studied the modulation of the electrically evoked release of [3H]5-HT by various 5-HT receptor agonists and antagonists in preloaded slices of human neocortex obtained from 18 patients undergoing neurosurgery. The nonselective 5-HT1A/1B/1D receptor agonist 5-carboxamidotryptamine produced a potent inhibition (70% at 0.03 μM) of the electrically evoked release of [3H]5-HT which was blocked by 5-HT receptor antagonists with the following relative order of potency: methiothepin 〉 metergoline = methysergide 〉 propranolol. The selective 5-HT1A receptor agonist 8-hydroxy-2–(di-n-propylamino)tetralin at 0.1 μM did not modify the electrically evoked release of [3H]5-HT. The 5-MT1A/1B receptor agonist RU 24969 was 10 times more potent at inhibiting [3H]5-HT overflow in the rat frontal cortex than in the human neocortex. The potent 5-HT1B receptor antagonist cyanopindolol did not modify the 5-carboxamidotryptamine-induced inhibition of the electrically evoked release of [3H]5-HT in slices of the human neocortex, but produced by itself a small inhibition of [3H]5-HT overflow. The α2-adrenoceptor antagonist yohimbine, which possesses affinity for the 5-HT1D receptor subtype, decreased the release of [3H]5-HT, but only in the presence of the selective α2-adrenoceptor antagonist idazoxan, which by itself increased significantly [3H]5-HT overflow. Taken together, these results support the view that the 5-HT receptor modulating the electrically evoked release of [3H]5-HT in slices of the human neocortex could be of the 5-HT1D subtype. Moreover, preliminary results obtained with idazoxan confirm the existence of a presynaptic α2-adrenoceptor modulating the release of [3H]5-HT in the human neocortex. These α2-heteroreceptors could exert a tonic inhibitory modulation on 5-HT neurotransmission in the human neocortex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08440.x
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  • 53
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    The Binding Properties of the Particulate and Solubilized Sulfonylurea Receptor from Cerebral Cortex Are Modulated by the Mg2+ Complex of ATP (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Glibenclamide closes an ATP-sensitive K+ channel (K-ATP channel) by interaction with the sulfonylurea receptor in the plasma membrane of pancreatic B cells and thereby initiates insulin release. Previous studies demonstrated that the Mg2+ complex of ATP decreases glibenclamide binding to the sulfonylurea receptor from pancreatic islets. The aim of the present study was to examine the effect of adenine and guanine nucleotides on binding of sulfonylureas to the cerebral sulfonylurea receptor. For this purpose, binding properties of the particulate and solubilized site from rat or pig cerebral cortex were analyzed. Maximum recovery of receptors in detergent extracts amounted to 40–50%. Specific binding of [3H]glibenclamide to the solubilized receptors corresponded well to specific binding to microsomes. In microsomes and detergent extracts, the Mg2+ complexes of ATP, ADP, GTP, and GDP inhibited binding of [3H]glibenclamide. These effects were not observed in the absence of Mg2+. In detergent extracts, Mg-ATP (300 μM) reduced the number of high-affinity sites for [3H]-glibenclamide by 52% and increased the dissociation constant for [3H]glibenclamide by eightfold; Mg-ATP was half-maximally effective at 41 μM. Alkaline phosphatase accelerated the reversal of Mg-ATP-induced inhibition of [3H]glibenclamide binding. The data suggest similar control of the sulfonylurea receptor from brain and pancreatic islets by protein phosphorylation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08444.x
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  • 54
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    Interactions Between Phospholipase C-Coupled and N-Methyl-D-Aspartate Receptors in Cultured Cerebellar Granule Cells: Protein Kinase C Mediated Inhibition of N-Methyl-D-Aspartate Responses (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The N-methyl-D-aspartate (NMDA) receptor of rat cerebellar granule cells in primary culture is inhibited by phospholipase C-coupled receptor activation. In the absence of ionotropic agonist, cells modulate their cytoplasmic free Ca2+, [Ca2+]c, in response to stimulation of M3 muscarinic receptors, metabotropic glutamate receptors, and endothelin receptors by the respective agonists carbachol, trans-l-amino-l,3-cyclopentanedicarboxylic acid, and endothelin-1. The response is consistent with the ability of phospholipase C-coupled receptors to release a pool of intracellular Ca2+ and induce a subsequent Ca2+ entry into the cell; both of these responses can be abolished by discharge of internal Ca2+ stores with low concentrations of ionomycin or thapsigargin. In the case of cells stimulated with NMDA, the [Ca2+]c response to the phospholipase C-coupled agonists is complex and agonist dependent; however, in the presence of ionomycin each agonist produces a partial inhibition of the NMDA component of the [Ca2+]c signal. This inhibition can be mimicked by the protein kinase C activator 4β-phorbol 12,13-dibutyrate. It is concluded that NMDA receptors on cerebellar granule cells are inhibited by phospholipase C-coupled muscarinic M3, glutamatergic, and endothelin receptors via activation of protein kinase C.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08339.x
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  • 55
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    Inhibition by Calmodulin Antagonists of [3H]MK-801 Binding in Brain Synaptic Membranes (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In brain synaptic membranes not extensively washed, (+)-5-[3H]methyl-10,1 l-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine ([3H]MK-801) binding was markedly inhibited in a concentration-dependent manner (at concentrations above 1 μM) by several compounds having antagonistic activity at the Ca2+-binding protein calmodulin. Scatchard analysis revealed that N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) inhibited the binding through a significant decrease in the density of binding sites without affecting the affinity at 10 μM. In membranes extensively washed and treated with a low concentration of Triton X-100, L-glutamic acid (Glu) drastically accelerated the initial association rate of [3H]MK-801 binding with glycine (Gly), almost doubling the initial association rate found in the presence of Glu alone. The addition of W-7 invariably reduced the initial association rate observed in the presence of either Glu alone or both Glu and Gly, without significantly altering the dissociation rate of bound [3H]-MK-801, irrespective of the presence of the two stimulatory amino acids. The maximal potencies of Glu, Gly, and spermidine in potentiating the binding were all attenuated by W-7. These results suggest that calmodulin antagonists may interfere with opening processes of an ion channel associated with an N-methyl-D-aspartate-sensitive subclass of excitatory amino acid receptors in rat brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08342.x
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  • 56
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    Extracellular Intermediates of Glucose Metabolism: Fluxes of Endogenous Lactate and Alanine Through Extracellular Pools in Embryonic Sympathetic Ganglia (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The flux rates of lactate and alanine in and out of the cells of an intact tissue, which cannot be measured directly because some of the released materials are reabsorbed, were determined by computer analysis of uptakes and outputs by the whole tissue in the presence of various concentrations of these substances. The outputs of labeled lactate and alanine from [U-14C]glucose and the uptakes of [U-14C]lactate and [U-14C]alanine were measured on intact sympathetic ganglia excised from 15-day-old chicken embryos. The volume and time constant of the extracellular space were measured using labeled lactate, alanine, and sucrose. Models, which mathematically described the cellular uptakes and outputs as functions of the extracellular concentrations, were used to predict the exchanges that would be observed on the whole tissue, and their parameters were adjusted for best fit to the actual observations. The fitted models were then used to calculate the fluxes in and out of the cells and the concentrations in the extracellular space. The following results were obtained: (1) Cellular uptakes of lactate and alanine were both well described by familiar Michaelis-Menten kinetics. (2) The cellular output of [14C]-lactate from [14C]glucose declined with increase in the extracellular lactate concentration, whereas the cellular output of [14C]alanine from [14C]glucose rose with the extracellular alanine concentration. (3) Half-saturation values for cellular uptake, determined from the fitted equations, were 0.45 mM for lactate and 1.17 mM for alanine, both several-fold lower than less relevant estimates for the whole tissue made directly from the uptake observations. (4) As much as 45% of the carbon in the glucose consumed was released into the extracellular space as lactate and alanine, but much of this was reabsorbed. Implications for brain metabolism are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08346.x
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  • 57
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    pp42/44MAP Kinase Is a Component of the Neurogenic Pathway Utilized by Nerve Growth Factor in PC12 Cells (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
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    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Nerve growth factor-stimulated mitogen-activated protein kinase (pp42/44MAP) kinase was characterized by sequential column chromatography on DEAE-Sephacel, phenyl-Sepharose CL4B, and S-200. The kinase displayed an apparent molecular mass of 42 kDa and reacted with an antiphosphotyrosine antibody. Peptide mapping of myelin basic protein revealed the presence of one phosphopeptide that was phosphorylated on Thr-97. pp42/44MAP kinase activity was dependent on Mg2+ and inhibited by K252a both in vitro and in vivo. Nerve growth factor-stimulated kinase activation was diminished by down-regulation of protein kinase C with 200 nM 12-phorbol 13-myristate acetate or with staurosporine (1 nM), a protein kinase C inhibitor. Genistein, a protein tyrosine kinase inhibitor, blocked nerve growth factor-mediated neurite extension as well as diminished activation of pp42/44MAP kinase. Our data demonstrate that activation of this kinase system by nerve growth factor displays a requirement for both protein kinase C as well as protein tyrosine kinase. In addition, other agents that are capable of promoting neurite outgrowth in PC12 cells, such as fibroblast growth factor or dibutryl cyclic AMP, do so independently of activating this kinase system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08352.x
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  • 58
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    A Novel Correlation Between the Levels of β-Amyloid Protein Precursor and τ Transcripts in the Aged Human Brain (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: β-Amyloid protein precursor (APP) and τ are implicated in the pathogenesis of Alzheimer's disease. We quantified the levels of APP and τ transcripts in the three cortical regions of 38 aged human brains obtained from consecutive autopsied patients. The level of APP mRNA was directly proportional to that of τ mRNA to a remarkable extent, suggesting coordinate expression of the APP and τ genes, whereas much weaker correlations were noted among mRNAs encoding other neuronal proteins. From the previous data on the differential expression of APP and τ mRNAs, the levels of APP-751 and -695 mRNAs were calculated and found to be proportional to those of four-repeat and three-repeat τ mRNAs, respectively, whereas that of APP-770 mRNA was rather constant. These results suggest that the mRNA concentrations of APP isoforms are linked to those of τ isoforms in the aged human brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08354.x
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  • 59
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    Evidence for the Implication of Phosphoinositol Signal Transduction in μ-Opioid Inhibition of DNA Synthesis (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: An opioid receptor agonist, [D-Ala2, Me-Phe4, Glyol5]enkephalin (DAMGE), decreased [3H]thymidine incorporation into DNA of fetal rat brain cell aggregates. This action proved to depend on the dose of this enkephalin analog and the interval the aggregates were maintained in culture. The opioid antagonist naltrexone and the μ-specific antagonist cyclic D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr amide (CTOP) reversed the DAMGE effect, arguing for a receptor-mediated mechanism. The μ-opioid nature of this receptor was further established by inhibiting DNA synthesis with the highly μ-selective agonist morphiceptin and blocking its action with CTOP. Several other opioids, pertussis toxin, and LiCl also diminished DNA synthesis, whereas cholera toxin elicited a modest increase. Naltrexone completely reversed the inhibition elicited by the combination of DAMGE and low doses of LiCl but not by that of high levels of LiCl alone. The enkephalin analog also reduced basal [3H]inositol trisphosphate and glutamate stimulated [3H]inositol monophosphate and [3H]inositol bisphosphate accumulation in the aggregates. These DAMGE effects were reversed by naltrexone and were temporally correlated with the inhibition of DNA synthesis. A selective protein kinase C inhibitor, chelerythrine, also in hibited thymidine incorporation dose-dependently. The effect of DAMGE was not additive in the presence of chelerythrine but appeared to be consistent with their actions being mediated via a common signaling pathway. These results suggest the involvement of the phosphoinositol signal transduction system in the modulation of thymidine incorporation into DNA by DAMGE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08357.x
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  • 60
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    Magnesium-Dependent Inhibition of Agonist-Stimulated Phosphoinositide Breakdown in Rat Cortical Slices by Excitatory Amino Acids (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The excitatory amino acid agonists kainate, N-methyl-D-aspartate (NMDA), and quisqualate inhibited ligand-stimulated phosphoinositide hydrolysis in rat cortical slices. The NMDA channel blocker MK-801 antagonized the inhibition by NMDA but had no effect on the inhibition due to kainate or quisqualate. The antagonist 6-cyano-7-nitroquinoxaline-2,3-dione blocked the effects of quisqualate and kainate but not the effect of NMDA. These data indicate that activation of the NMDA, α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid, and kainate types of ionotropic receptors has the same effect. In membranes prepared from cortical slices, there was no inhibition of carbachol-stimulated phosphoinositidase C activity by excitatory amino acids, suggesting that excitatory amino acids indirectly affect carbachol-stimulated phosphoinositide hydrolysis. The inhibition by excitatory amino acids of carbachol-stimulated phosphoinositide breakdown was dependent on extracellular Mg2+ and was abolished by procedures that increase intracellular Ca2+. Veratridine inhibition of carbachol-stimulated phosphoinositide hydrolysis was reversed by ouabain but not by other procedures that increase intracellular Ca2+. In contrast to excitatory amino acids, veratridine potentiated carbachol-stimulated phosphoinositide breakdown in the presence of 10 mM extracellular Mg2+. These data suggest that excitatory amino acids inhibit carbachol-stimulated phosphoinositide breakdown in rat cortex by lowering intracellular Ca2+ through a mechanism dependent on extracellular Mg2+.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08336.x
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    Quantitation of Rat Dopamine Transporter mRNA: Effects of Cocaine Treatment and Withdrawal (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Dopamine transporter mRNA levels in the rat substantia nigra were quantified using a sensitive nuclease protection assay with a highly homologous human dopamine transporter cDNA clone. The same probe was also used to visualize dopamine transporter mRNA in the substantia nigra by in situ hybridization. Repeated cocaine administration (15 mg/kg, twice a day for 6.5 days) resulted in a 〉40% decrease in nigral dopamine transporter mRNA levels. In contrast, dopamine transporter mRNA levels were unchanged after either acute treatment (4 h before death) or repeated cocaine treatment followed by a 72-h withdrawal period. Thus, blockade of the dopamine transporter by repeated cocaine administration may result in the down-regulation of dopamine transporter gene expression in dopamine neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08365.x
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    Homeostatic Role for γ-Aminobutyric Acid in the Brain (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08367.x
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    Differential Effects of Insulin on Choline Acetyltransferase and Glutamic Acid Decarboxylase Activities in Neuron-Rich Striatal Cultures (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We studied the effects of insulin, nerve growth factor (NGF), and tetrodotoxin (TTX) on cellular metabolism and the activity of glutamic acid decarboxylase (GAD) and choline acetyltransferase (ChAT) in neuron-rich cultures prepared from embryonic day 15 rat striatum. Insulin (5 μg/ml) increased glucose utilization, protein synthesis, and GAD activity in cultures plated over a range of cell densities (2,800-8,400 cells/mm2). TTX reduced GAD activity; NGF had no effect on GAD activity. Insulin treatment reversibly reduced ChAT activity in cultures plated at densities of 〉4,000 cells/mm2, and the extent of this reduction increased with increasing cell density. The number of acetylcholinesterase-positive neurons was not reduced by insulin, suggesting that insulin acts by down-regulating ChAT rather than by killing cholinergic neurons. Insulin-like growth factor-1 (IGF-1) reduced ChAT activity at concentrations 10-fold lower than insulin, suggesting that insulin's effect on ChAT may involve the IGF-1 receptor. NGF increased ChAT activity; TTX had no effect on ChAT activity. These results suggest that striatal cholinergic and GABAergic neurons are subject to differential trophic control.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09387.x
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    Dynamic Observation of Dopamine Autoreceptor Effects in Rat Striatal Slices (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Fast-scan cyclic voltammetry has been used to measure dopamine (DA) synaptic overflow in slices of rat caudate nucleus induced by electrical stimulation with one-, two-, and 50-pulse, 10-Hz trains. Synaptic overflow in this preparation is shown to be the result of the competing effects of release and cellular uptake. Release caused by all pulses was attenuated by the D2 agonist quinpirole (1 μM). The rapid time response of the measurements (100 ms) allows the autoinhibition induced by endogenous, released DA to be resolved in real time. The concentration of DA released during the second pulse of a train was 58% of that released by the first pulse, an effect that is partially blocked by the addition of 2 μM sulpiride, a D2 antagonist, to the perfusion buffer. DA release during the first stimulus pulse is unaffected by 2 μM sulpiride, suggesting that autoreceptors are not normally occupied in this preparation. Release caused by the third pulse was 14% of the first pulse and also could be partially enhanced by 2 μM sulpiride. The duration of the inhibition of release induced by endogenous DA was estimated by varying the interval between one-pulse stimulations until the overflow of DA induced by the second pulse was equal to that on the first; a half-time of ∼ 17 s was found. The addition of picrotoxin (100 μM) and glutamate (10 μM) to the perfusion buffer did not affect stimulated release of DA, although the addition of atropine (100 μM) attenuated overflow for all the trains tested.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09391.x
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  • 65
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    Enhancement of Endogenous Release of Glutamate and γ-Aminobutyric Acid from Hippocampus CA1 Slices After In Vivo Long-Term Potentiation (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of long-term potentiation (LTP) on endogenous amino acid release from rat hippocampus slices was studied. LTP was induced in vivo by application of a tetanus (200 Hz, 200 ms) to the Schaffer collateral fibers in unanesthetized rats. Endogenous release of glutamate and γ-aminobutyric acid (GABA) was investigated 60 min after tetanization in CA1 subslices of potentiated and control rats. No significant effects of LTP were observed in basal and K+-induced Ca2+-independent release components of these amino acids. In contrast, K+-induced Ca2+-dependent release of both glutamate and GABA increased ∼ 100% in slices from potentiated rats. No differences were observed in total content of glutamate and GABA between the subslices from control and LTP animals. These results suggest a persistent increase in the recruitment of the presynaptic vesicular pool of glutamate and GABA during LTP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09395.x
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  • 66
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    Binding Properties of 3-[125I]Iodophencyclidine, a New Radioligand for N-Methyl-D-Aspartate-Gated Ionic Channels (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The binding properties of the 125l-labeled phencyclidine derivative N-[1-(3-[125I] iodophenyl)cyclohexyl] piperidine (3-[125I]iodo-PCP), a new ligand of the N-methyl-D-aspartate (NMDA)-gated ionic channel, were investigated. Association and dissociation kinetic curves of 3-[125I]iodo-PCP with rat brain homogenates were well described by two components. About 32% of the binding was of fast association and fast dissociation, and the remaining binding was of slow association and slow dissociation. Saturation curves of 3-[125I] iodo-PCP also were well described using two binding sites: one of a high affinity (KDH= 15.8 ± 2.3 nM) and the other of a low affinity (KDL= 250 ± 40 nM). 3-Iodo-PCP inhibited the binding of 3-[125I]iodo-PCP with inhibition curves that were well fitted by a two-site model. The binding constants (KiH, BmaxH; KiL, BmaxL) so obtained were close to those obtained in saturation experiments. Ligands of NMDA-gated ionic channels also inhibited the binding of 3- [125I]iodo-PCP with two constants, KiH and KiL. There was a very good correlation (r = 0.987) between the affinities of these ligands to bind to NMDA-gated ionic channels and their potencies to inhibit the binding of 3-[125I]iodo-PCP with a high affinity. Moreover, the regional distribution of the high-affinity binding of 3-[125I]-iodo-PCP paralleled that of tritiated N-[1-(2-thienyl)cyclohexyl]piperidine ([3H]TCP). In contrast to that of [3H]TCP, the binding of 3-[125I]iodo-PCP to well-washed rat brain membranes was fast and insensitive to glutamate and glycine. We conclude that 3-[125I]iodo-PCP, at low concentrations, is suited for future rapid autoradio-graphical studies of both open and closed forms of NMDA-gated ionic channels and that 3-[123I]iodo-PCP could be used successfully for in vivo studies by single-photon emission computed tomography analysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09397.x
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    Mobilization of the Readily Releasable Pool of Acetylcholine from a Sympathetic Ganglion by Tityustoxin in the Presence of Vesamicol (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The present experiments tested whether preganglionic stimulation and direct depolarization of nerve terminals by tityustoxin could mobilize similar or different pools of acetylcholine (ACh) from the cat superior cervical ganglia in the presence of 2-(4-phenylpiperidino)cyclohexanol (vesamicol, AH5 183), an inhibitor of ACh uptake into synaptic vesicles. In the absence of vesamicol, both nerve stimulation and tityustoxin increased ACh release. In the presence of vesamicol, the release of ACh induced by tityustoxin was inhibited, and just 16% of the initial tissue content could be released, a result similar to that obtained with electrical stimulation under the same condition. When the impulse-releasable pool of ACh had been depleted, tityustoxin still could release transmitter, amounting to some 10% of the ganglion's initial content. This pool of transmitter seemed to be preformed in the synaptic vesicles, rather than synthesized in response to stimuli, as tityustoxin could not release newly synthesized [3H]ACh formed in the presence of vesamicol, and hemicholinium-3 did not prevent the toxin-induced release. In contrast to the results with tityustoxin, preganglionic stimulation could not release transmitter when impulse-releasable or toxin-releasable compartments had been depleted. Our results confirm that vesamicol inhibits the mobilization of transmitter from a reserve to a more readily releasable pool, and they also suggest that, under these experimental conditions, there might be some futile transmitter mobilization, apparently to sites other than nerve terminal active zones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09404.x
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    Amino Acid Release from Cerebral Cortex in Experimental Acute Liver Failure, Studied by In Vivo Cerebral Cortex Microdialysis (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Both increased γ-aminobutyric acid (GABA)-ergic and decreased glutamatergic neurotransmission have been suggested relative to the pathophysiology of hepatic encephalopathy. This proposed disturbance in neurotransmitter balance, however, is based mainly on brain tissue analysis. Because the approach of whole tissue analysis is of limited value with regard to in vivo neurotransmission, we have studied the extracellular concentrations in the cerebral cortex of several neuroactive amino acids by application of the in vivo microdialysis technique. During acute hepatic encephalopathy induced in rats by complete liver ischemia, increased extracellular concentrations of the neuroactive amino acids glutamate, taurine, and glycine were observed, whereas extracellular concentrations of aspartate and GABA were unaltered and glutamine decreased. It is therefore suggested that hepatic encephalopathy is associated with glycine potentiated glutamate neurotoxicity rather than with a shortage of the neurotransmitter glutamate. In addition, increased extracellular concentration of taurine might contribute to the disturbed neurotransmitter balance. The observation of decreasing glutamine concentrations, after an initial increase, points to a possible astrocytic dysfunction involved in the pathophysiology of hepatic encephalopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09410.x
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    Excitatory Amino Acid-Induced Phosphoinositide Turnover in Guinea Pig Cerebral Cortical Slices: Selective Enhancement by Spermine of the Response to DL-1-Aminocyclopentane- trans-1, 3-Dicarboxylate (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In the presence of 1 mM spermine, accumulations of 3H labelled inositol phosphates elicited by quisqualate (100 μM) and 1 -aminocyclopentane-trans- 1, 3-dicarboxylate (t-ACPD, 300 μM) were significantly enhanced by 21 and 26%, respectively, without a significant alteration in the accumulation elicited by l-glutamate (10 mM) or DL-α-amino-3-hydroxy-5-methyl-4-isoxalone propionate (10 μM). Analysis of concentration-response data indicated that the presence of spermine led to an increase in the maximal response to t-ACPD without altering the EC50 value. The stimulatory effect of spermine on the accumulation of t-ACPD-elicited 3H-inositol phosphates was not reversed by ifenprodil or diethylenetriamine (putative polyamine site antagonists), by agents that activate or inhibit protein kinase C, or by calcium channel blockade, but was abolished in the presence of elevated extracellular calcium ion concentration. We conclude that spermine enhances the phosphoinositide turnover in guinea pig cerebral cortical slices elicited by the “metabotropic” excitatory amino acid receptor. The site through which the action of spermine is mediated remains to be defined, but it is apparently distinct from that suggested to modulate N-methyl-D-aspartate receptor activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09413.x
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  • 70
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    Neuronal Ganglioside Increases Dependent on the Neuron-Glia Interaction in Primary Culture (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Dissociated neuronal cells from rat embryonic hemispheres were cultivated on astroglial layers. The increase in ganglioside content of the cocultures was more rapid than that of neuronal cultures seeded on polylysine surfaces for the first 24 h, and the extent of the increase was greater 7 days after inoculation, probably because of interaction between the preformed astroglial layers and the neuronal cells in vitro. The promoted expression of the a-pathway gangliosides, GM1 and GD la, was recognized by TLC and the increase in GM 1 was immunologically ascertained. The incorporation of 3H-labeled N-acetyl-D-mannosamine into GD3 and b-series gangliosides was elevated for the first 24 h. However, cocultures in which there was no contact between neuronal cells and the astroglial sheet showed no appreciable increase in incorporation. Thus, cell surface changes were induced at the membrane glycolipid level in the neuronal cells by contact with astroglial layers. The synthesis and expression of neuronal gangliosides are discussed in relation to the onset of neuron-glia interaction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09417.x
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    The Postsynaptic Density: Constituent and Associated Proteins Characterized by Electrophoresis, Immunoblotting, and Peptide Sequencing (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The proteins of the postsynaptic density (PSD) fraction of cerebral cortex were resolved by two-dimensional electrophoresis (2DE) and more than 30 proteins identified by characteristic 2DE mobility, immunoblotting with specific antibodies, and N-terminal and peptide sequencing. The PSD fraction is enriched for spectrin, actin, tubulin and microtubule associated protein II, myosin, enzymes of glycolysis, creatine kinase, elongation factor 1α, and receptor protein. The three neurofilament proteins are detected but a 58-kDa protein is prominent and is, by peptide sequencing, the bovine homolog of the recently cloned 66-kDa neurofilament protein; in contrast to the latter, however, it is enriched in cerebrum compared with spinal cord. A 68-kDa protein is identified as a member of the hsp70/ BiP family of proteins. A protein, designated dynamin, indicating its putative role as a microtubule motor, is identified as a major protein, is found, however, greatly enriched in the particulate fraction, and is significantly denaturant and detergent insoluble. A protein designated N-ethylmale-imide-sensitive factor is also detected. Thus, two proteins implicated in vesicular transport are present in the PSD fraction. Seven polyclonal antibodies were produced to 2DE separated and electroeluted proteins of the PSD and were identified by peptide sequence analysis and 2DE profile as the hsp70/BiP homologous protein, the novel neurofilament protein synapsin IIa, pyruvate kinase, dynamin, aconitase and an unknown contaminating protein, and a 115-kDa protein that by subcellular fractionation and immunoblotting is a diagnostic PSD molecule. In addition, peptide sequences are obtained for four additional higher molecular weight proteins of the PSD that are not related at the level of primary structure to any known proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09421.x
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    Binding and Active Transport of Large Analogues of Acetylcholine by Cholinergic Synaptic Vesicles In Vitro (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: A previous structure-activity investigation of acetylcholine (ACh) revealed a positive correlation between additional hydrophobic bulk and increased potency for inhibition of active transport of [3H]ACh by synaptic vesicles isolated from the electric organ of Torpedo. In the current study, several ACh analogues that are significantly larger than previously studied “false transmitters” were synthesized in the tritiated form by chemical means and tested for active transport. These are analogue 14 [(±)-(cis,trans)-1-benzyl-1-methyl-3-acetoxypyrrolidinium iodide], analogue 15 [(±)-1,1-dimethyl-3-benzoyloxypyrrolidinium iodide], and analogue 16/17 [(±)-(cis,trans)- 1-benzyl-1-methyl-3-benzoyloxypyrrolidinium iodide]. These analogues place significant additional hydrophobic bulk on one or the other (analogues 14 and 15) or both (analogue 16/17) of the two pharmacophores of a small, conformationally constrained analogue of ACh. [3H]Analogue 14 and [3H]analogue 15 are actively transported, with Vmax values the same as or less than that of ACh, depending on the vesicle preparation. The observation that Vmax is the same for an analogue and ACh in some vesicle preparations suggests that the rate-limiting step does not involve ACh bound to the transporter. [3H]-Analogue 16/17 is actively transported very poorly. Km values for ACh and for transported ACh analogues vary by up to two- to threefold in different vesicle preparations. The ACh transporter is much less selective for transported substrates than anticipated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09424.x
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    MK-801 Prevents 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinsonism in Primates (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In cynomologus monkeys, systemic administration of MK-801, a noncompetitive antagonist for the N-methyl-4-aspartate receptor, prevented the development of the parkinsonian syndrome induced by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). MK-801 also attenuated dopamine depletion in the caudate and putamen and protected dopaminergic neurons in the substantia nigra from the degeneration induced by the neurotoxin. Nevertheless, 7 days after MPTP administration in the caudate and putamen of monkeys also receiving MK-801, the levels of toxic l-methyl-4-phenylpyridinium were even higher than those measured in monkeys receiving MPTP alone. This indicates that the protective action of MK-801 is not related to MPTP metabolism and strongly suggests that, in primates, the excitatory amino acids could play a crucial role in the mechanism of the selective neuronal death induced by MPTP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09429.x
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    Brain Levels of Microtubule-Associated Protein τ Are Elevated in Alzheimer's Disease: A Radioimmuno-Slot-Blot Assay for Nanograms of the Protein (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The microtubule-associated protein τ which stimulates the assembly of α-β tubulin heterodimers into microtubules, is abnormally phosphorylated in Alzheimer's disease (AD) brain and is the major component of paired helical filaments. In the present study, the levels of τ and abnormally phosphorylated τ were determined in brain homogenates of AD and age-matched control cases. A radioimmuno-slot-blot assay was developed, using a primary monoclonal antibody, Tau-1, and a secondary antibody, antimouse 125I-immunoglobulin G. To assay the abnormally phosphorylated τ, the blots were treated with alkaline phosphatase before immunolabeling. The levels of total τ were about eightfold higher in AD (7.3 ± 2.7 ng/μg of protein) than in control cases (0.9 ± 0.2 ng/μg), and this increase was in the form of the abnormally phosphorylated protein. These studies indicate that the abnormal phosphorylation—not a decrease in the level of τ—is a likely cause of neurofibrillary degeneration in AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09432.x
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    Analysis of Muscarinic Receptor Subtypes in the Mouse Cochlea by Means of the Polymerase Chain Reaction (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Total RNA was extracted with guanidine thiocyanate from the cochleas of 16-day-old CBAJ mice. The mRNA was purified from the total RNA using oligo-dT cellulose, and the mRNA was treated with DNase to degrade genomic DNA. After reverse transcription, resulting cDNA was amplified by polymerase chain reaction (PCR), using primers specific for the nucleotide sequences m1-m5, representing subtypes of muscarinic acetylcholine receptors. PCR products corresponding to subtypes m1, m3, and m5, but not to m2 and m4, were amplified. These results suggest that muscarinic acetylcholine receptors of these odd-numbered subtypes are expressed in the mammalian cochlea.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb09436.x
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    Specific Expression of N-Acetylaspartate in Neurons, Oligodendrocyte-Type-2 Astrocyte Progenitors, and Immature Oligodendrocytes In Vitro (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To test the specificity of N-acetylaspartate (NAA) as a neuronal marker for proton nuclear magnetic resonance (1H NMR) spectroscopy, purified and characterized cultured cells were analyzed for their NAA content using both 1H NMR and HPLC. Cell types studied included cerebellar granule neurons, type-1 astrocytes, meningeal cells, oligodendrocyte-type-2 astrocyte (O–2A) progenitor cells, and oligodendrocytes. A high concentration of NAA was found in extracts of cerebellar granule neurons (approximately 12 nmol/mg of protein), whereas NAA remained undetectable in purified type-1 astrocytes, meningeal cells, and mature oligodendrocytes. However, twice the neuronal level of NAA was found in O-2A progenitors grown in vitro. In addition significant levels of NAA were also detected in cultures of immature oligodendrocytes. Our data partly support previous suggestions that NAA may be a useful neuronal marker for 1H NMR spectroscopic examination of the adult brain. However, they also raise the further possibility that alterations of NAA associated with some specific brain disorders, particularly disorders seen in newborn and young children, may reflect abnormalities in the development of oligodendroglia or their precursors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08875.x
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    Distinct Developmental Patterns of Expression of Rat α1, α5, γ2S, andα12Lγ-Aminobutyric AcidA Receptor Subunit mRNAs In Vivo and In Vitro (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have quantitated the α1, α5, γ2S, and γ2Lγ-aminobutyric acidA (GABAA) receptor subunit mRNAs in the maturing cerebellum in vivo and in cerebellar granule neurons differentiating in vitro. Absolute amounts of mRNA were measured by reverse transcription and competitive polymerase chain reaction (PCR) analysis with appropriate internal standards. The α1 and γ2L mRNA content increased continuously during postnatal cerebellar maturation and their changes with time matched very closely those of the cerebellar granule cells differentiating in vitro. The γ2S subunit mRNA showed a relatively constant pattern of expression both in vivo and in vitro, with comparable absolute concentrations in both developmental paradigms. The α5 mRNA was initially high in vivo and decreased (eightfold) to adult levels as postnatal cerebellar development progressed. In vitro the amount of α5 GABAA receptor subunit mRNA was higher than in vivo at 3 days, increased by more than twofold by 8 days, and declined to approximately the initial values at 23 and 28 days in vitro. Collectively, the results indicate that the α1, α5, γ2S, and γ2L GABAA receptor subunit mRNAs are regulated differentially in a temporal manner during in vivo and in vitro maturation. Moreover, a comparison of the ontogenetic profiles of the γ2S and γ2L mRNAs indicates that alternative splicing of the γ2 primary RNA transcript is regulated developmentally during postnatal maturation of the rat cerebellum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08876.x
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    Effect of Intracellular Glutamine on the Uptake of Large Neutral Amino Acids in Astrocytes: Concentrative Na+-Independent Transport Exhibits Metastability (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: To examine whether the concentration gradient of glutamine (Gln) drives concentrative Na+-independent uptake of neutral amino acids (NAA) in mouse cerebral astrocytes, uptake was compared in “Gln-depleted” and “Gin-replete” cultures. Uptake (30 min in Na+-free buffer) of histidine, kynurenine, leucine, tyrosine, and a model substrate for System L transport was 70–150% greater in Gin-replete cultures. Phenylalanine uptake was not affected. All of these NAA trans-stimulated the export of Gln from astrocytes. However, the increase in NAA uptake was sustained even though the Gln content of Gin-replete cultures declined. Also, uptake of Gln itself was enhanced in Gln-re-plete cultures. Thus, countertransport of Gln was insufficient to explain the enhancement of NAA uptake. Enhanced uptake was restored, and could be magnified, by reloading Gin-depleted cultures either with Gln or with histidine. It is suggested that substrate-induced asymmetry and molecular hysteresis in the Na+-independent carrier could account for the sustained enhancement of NAA uptake. Only histidine and kynurenine were concentrated comparably to Gin (15- to 29-fold at 1 mM in Na+-free buffer). The other NAA were four to six times less concentrated. At least two Na+-dependent transport systems also supported the concentration gradient of Gln in regular buffer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08895.x
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  • 79
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    Cell Swelling, Blebbing, and Death Are Dependent on ATP Depletion and Independent of Calcium During Chemical Hypoxia in a Glial Cell Line (ROC-1) (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The morphological and biochemical changes that occur during chemical hypoxic injury in a neural cell line were studied in the presence and absence of calcium. Oligo-dendroglial-glioma hybrid cells (ROC-1) were subjected to inhibitors of glycolytic and oxidative ATP synthesis (chemical hypoxia). Complete respiratory inhibition depleted [ATP] to 〈5% of control by 4 min. Blebs appeared on the cell surfaces and cells began to swell within a few minutes of ATP depletion. A 200% increase in cell volume and bleb coalescence preceded irreversible cell injury (lactate dehy-drogenase release) which began at ∼20 min with 50% cell death by 40 min. In energized cells an equivalent degree of osmotic swelling induced by ouabain inhibition of the Na+, K+-ATPase pump did not produce blebbing or cell death. Partial inhibition of respiration decreased [ATP] to ∼10% of control by 40 min. Blebbing and swelling began at 40 min and bleb coalescence preceded plasma membrane disruption which began at ∼55 min. ATP depletion, blebbing, swelling, and death followed similar time courses in the presence or absence of extracellular calcium ([Ca2+]e). Intracel-lular calcium ([Ca2+]i) was measured using fura-2. In calcium-containing medium metabolic inhibition caused a transient increase in resting [Ca2+]i (100 ± 17 nM) followed by a low steady-state level preceding plasma membrane disruption. Following deenergization in calcium-free medium, [Ca2+]i remained below 60 nM throughout injury and death. These data suggest that decreased ATP initiates a sequence of events including bleb formation and cell swelling that lead to irreversible cell injury in the absence of large increases in [Ca2+]i.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08910.x
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  • 80
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    Glutamate Release in Experimental Ischaemia of the Retina: An Approach Using Microdialysis (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A rabbit eye model of neural ischaemia is described that uses an increased pressure in the anterior eye chamber to block the capillary supply to the retina. A microdialysis probe placed very close to the retinal surface was used to monitor release of amino acids during ischaemia. A large (two- to threefold) increase in the release of glutamate and O-phosphoserine (twofold), but not of six other amino acids monitored, occurred during initial ischaemia. During reperfusion after release of intraocular pressure, much larger (five- to 10-fold) increases in the release of these amino acids were observed. Parallel ischaemic retinal tissue damage was observed. This damage was prevented by keta-mine applied locally via a superfusion needle, suggesting that glutamate released during ischaemia, and particularly during reperfusion, was responsible for cell death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08912.x
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  • 81
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    Activation of Metabotropic Glutamate Receptors in the Hippocampus Increases Cyclic AMP Accumulation (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The selective metabotropic glutamate receptor agonist trans-1-aminocyclopentane-1,3-dicarboxylic acid (trans-ACPD) stimulates phosphoinositide hydrolysis and elicits several physiological responses in rat hippocampal slices. However, recent studies suggest that the physiological effects of trans-ACPD in the hippocampus are mediated by activation of a receptor that is distinct from the phosphoinositide hydrolysis-linked receptor. Previous experiments indicate that cyclic AMP mimics many of the physiological effects of trans-ACPD in hippocampal slices. Furthermore, recent cloning and biochemistry experiments indicate that multiple metabotropic glutamate receptor subtypes exist, some of which are coupled to yet unidentified effector systems. Thus, we performed a series of experiments to test the hypothesis that ACPD increases cyclic AMP levels in hippocampal slices. We report that 1S,3R- and 1S,3S-ACPD (but not 1R,3S-ACPD) induce a concentration-dependent increase in cyclic AMP accumulation in hippocampal slices. This effect was blocked by the metabotropic glutamate receptor antagonist L-2-amino-3-phosphonoproprionic acid but not by selective antagonists of ionotropic glutamate receptors. Furthermore, our results suggest that 1R,3S-ACPD-stimulated increases in cyclic AMP accumulation are not secondary to increases in cell firing or to activation of phosphoinositide hydrolysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08914.x
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  • 82
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    Avian Brain Epinephrine and 5-Hydroxytryptamine: Is It Still a Matter of Controversy? (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08917.x
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  • 83
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    REPLY FROM M. L. DUBOCOVICH, J. A. SIUCIAK, AND P. H. GAMACHE (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08918.x
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  • 84
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    Correction (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08922.x
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  • 85
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    Biochemical and Functional Properties of Somatostatin Receptors (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10938.x
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  • 86
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    Effects of Choline and Quiescence on Drosophila Choline Acetyltransferase Expression and Acetylcholine Production by Transduced Rat Fibroblasts (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Rat-1 fibroblasts were transduced to express Drosophila choline acetyltransferase. The presence of an active enzyme in these cells (Rat-1/dChAT) was confirmed using various methods. Rat-1/dChAT fibroblasts released acetylcholine (ACh) into the culture medium. Moreover, intra-and extracellular levels of ACh could be increased by adding exogenous choline chloride. In addition, serum starvation or confluence-induced quiescence caused an 80% decrease in recombinant choline acetyltransferase activity (compared with actively growing cells). ACh release was also repressed in quiescent fibroblast cultures. Exogenous choline could mitigate the decrease in ACh release. These results indicate that Rat-1 fibroblasts can be genetically modified to produce ACh and that ACh release can be controlled by introducing choline into the culture medium. Furthermore, these data demonstrate that the expression of the retroviral promoter used in this study decreases with the onset of quiescence; however, exogenous choline can increase the amount of ACh released by quiescent fibroblasts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10942.x
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  • 87
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    Glucocorticoids Exacerbate Hypoxic and Hypoglycemic Hippocampal Injury In Vitro: Biochemical Correlates and a Role for Astrocytes (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The acute secretion of glucocorticoids is critical for responding to physiological stress. Under normal circumstances these hormones do not cause acute neuronal injury, but they have been shown to enhance ischemic and seizure-induced neuronal injury in the rat brain. Using fetal rat hippocampal cultures, we asked whether hypoxic and hypoglycemic cell damage in vitro could be exacerbated by direct exposure to corticosterone (CORT). Each of these insults alone damaged neuronal cells, whereas 4–6 h of hypoxic treatment could damage age-matched astrocytes if glucose was reduced or omitted. Ischemic-like injury to both cell types could be attenuated by pretreatment with high (30 mM) glucose. Exposure to 100 nM CORT did not affect cell viability under control conditions but enhanced both hypoxic and hypoglycemic neuronal injury. In both cases, pretreatment with high glucose abolished this CORT-mediated synergy. In astrocyte cultures, CORT exacerbated both hypoxic and hypoglycemic injury and this effect was also attenuated by high-glucose pretreatment. Identical 24-h CORT treatment caused a 13% reduction in glucose uptake in astrocytes and a 38% reduction in glycogen content, without affecting the level of intracellular glucose. Thus, CORT could endanger both neurons and astrocytes in mixed hippocampal cultures and this effect emerged only under conditions of substrate depletion. The metabolic disruption in astrocytes by CORT further suggests that the ability of CORT to exacerbate neuronal injury may be due in part to impaired glial cell function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08884.x
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  • 88
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    A Molecular Mechanism for the Induction of Neurofilament Bundling by Aluminum Ions (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Al induces neurofibrillary tangles in the perikaryon of neurons in vivo and in culture. The effect of Al ions complexed with maltol, a plant-derived ligand of Al, on purified neurofilament preparations was studied in vitro. The binding of Al to the arm-like projections of the high (H)- and medium (M)-molecular-weight neurofilament subunits causes a conformational change of the molecule (intrafilamentous reaction), characterized by an altered migration on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). In addition, Al compounds strongly stimulate the interaction between neurofilaments (interfilamentous reaction). The possibility that phosphate groups of the H and M sidearms are involved in binding Al ions is discussed with regard to the migration on SDS-PAGE of dephosphorylated neurofilaments incubated with Al compounds and the alteration by Al ions of neurofilament phosphorylation in vitro by the associated kinase. Immunoblotting analysis of neurofilaments in cultivated neurons intoxicated with Al compounds revealed a similar Al-dependent alteration of the neurofilament subunit conformation. This result suggests that the mechanism of Al-induced bundling of neurofilaments derived from in vitro studies might be involved in the formation of tangles in situ.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10947.x
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  • 89
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    Inhibition of Tyrosine Hydroxylase by R and S Enantiomers of Salsolinol, 1-Methyl-6,7-Dihydroxy-1,2,3,4- Tetrahydroisoquinoline (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Salsolinol is one of the dopamine-derived tetrahydroisoquinolines and is synthesized from pyruvate or acetaldehyde and dopamine. As it cannot cross the blood-brain barrier, salsolinol as the R enantiomer in the brain is considered to be synthesized in situ in dopaminergic neurons. Effects of R and S enantiomers of salsolinol on kinetic properties of tyrosine hydroxylase [tyrosine, tetrahydrobiopterin:oxygen oxidoreductase (3-hydroxylating); EC 1.14.16.2], the rate-limiting enzyme of catecholamine biosynthesis, were examined. The naturally occurring co-factor of tyrosine hydroxylase, l-erythro-5,6,7,8-tetra-hydrobioptein, was found to induce allostery to the enzyme polymers and to change the affinity to the biopterin itself. Using l-erythro-5,6,7,8-tetrahydrobiopterin, tyrosine hydroxylase recognized the stereochemical structures of the salsolinols differently. The asymmetric center of salsolinol at C-1 played an important role in changing the affinity to l-tyrosine. The allostery of tyrosine hydroxylase toward biopterin cofactors disappeared, and at low concentrations of biopterin such as in brain tissue, the affinity to the cofactor changed markedly. A new type of inhibition of tyrosine hydroxylase, by depleting the allosteric effect of the endogenous biopterin, was found. It is suggested that under physiological conditions, such a conformational change may alter the regulation of DOPA biosynthesis in the brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10951.x
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  • 90
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    Stimulus-Induced Accumulation of Inositol Tetrakis-, Pentakis-, and Hexakisphosphates in N1E-115 Neuroblastoma Cells (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: When [3H]inositol-prelabelled N1E-115 cells were stimulated with carbamylcholine (CCh) (100 μM), high K+ (60 mM), and prostaglandin E, (PGE,) (10 μM), a transient increase in [3H]inositol pentakisphosphate (InsP5) accumulation was observed. The accumulation reached its maximum level at 15 s and had declined to the basal level at 2 min. CCh, high K+, and PGE, also caused accumulations of [3H]inositol 1,4,5-trisphosphate [Ins(1,4,5)P3], [3H]inositol 1,3,4,6-tetrakisphosphate [Ins(1,3,4,6)P4], and 13H]inositol hexakisphosphate (InsP6). Muscarine and CCh induced accumulations of [3H]Ins(1,4,5)P3, [3H]-Ins(1,3,4,6)P4, [3H]InsP5, and [3H]InsP6 with a similar potency and exerted these maximal effects at 100 μM, whereas nicotine failed to do so at 1 mM. With a slower time course, CCh, high K+, and PGE1 caused accumulations of [3H]-inositol 1,3,4-trisphosphate [Ins(1,3,4)P3] and [3H]inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4]. In an N1E-115 cell homogenate, [3H]Ins(1,4,5)P3, [3H]Ins(1,3,4,5)P4, and [3H]Ins(1,3,4)P3 were converted to [3H]InsP5 through [3H]-Ins(1,3,4,6)P4. The above results indicate that Ins(1,3,4,6)P4, InsP5, and InsP6 are rapidly formed by several kinds of stimulants in N1E-115 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10953.x
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  • 91
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    A Dihydropyridine-Resistant Component in the Rat Adrenal Secretory Response to Splanchnic Nerve Stimulation (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
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    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: A study of the effects of dihydropyridine Ca2+ channel modulators on the release of catecholamines from perfused rat adrenal glands, evoked by electrical stimulation of their splanchnic nerves, is presented. Electrically mediated secretory responses were compared to chemically mediated responses (exogenous acetylcholine, nicotine, or high K+). Intensities of stimuli were selected to produce quantitatively similar secretory responses (between 100 and 200 ng per stimulus). The main finding of the study is that responses to transmural stimulation (300 pulses at 1 or 10 Hz) and to acetylcholine were inhibited only partially (about 50%) by isradipine, an L-type Ca2+ channel blocker. In contrast, responses to high K+ (17.5 mM for 2 min) were highly sensitive to isradipine (IC50= 8.2 nM). Responses to nicotine were also fully inhibited by this drug. Bay K 8644 (an L-type Ca2+ channel activator) potentiated mildly the secretory responses to electrical stimulation at 10 Hz and to acetylcholine, but increased threefold the responses to K+ and nicotine. It is, therefore, likely that responses mediated by high K+ or nicotinic receptors are triggered by external Ca2+ gaining access to the internal secretory machinery through L-type, dihydropyridine-sensitive voltage-dependent Ca2+ channels. However, in addition to nicotinic receptors, the physiological stimulation of adrenal medulla chromaffin cells through splanchnic nerves has other components, i.e., muscarinic receptor stimulation or the release of cotransmitters such as vasoactive intestinal polypeptide. The poorer sensitivity to dihydropyridines of secretory responses triggered by electrical stimulation of splanchnic nerve terminals or exogenous acetylcholine speaks in favor of alternative Ca2+ pathways, probably some dihydropyri-dine-resistant Ca2+ channels, in modulating the physiological adrenal catecholamine secretory process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10956.x
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  • 92
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    Concerted CMP-Dependent [3H]Inositol Labeling of Phosphoinositides and Agonist Activation of Phospholipase C in Rat Brain Cortical Membranes (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: [3H]Inositol ([3H]Ins) labeling of phosphoinositides was studied in rat brain cortical membranes. [3H]Ins was incorporated into a common lipid pool through both CMP-dependent and independent mechanisms. These are as follows: (1) a reverse reaction catalyzed by phosphatidyl-inositol (PtdIns) synthase, and (2) the reaction performed by the PtdIns headgroup exchange enzyme, respectively. Membrane phosphoinositides prelabeled in either CMP-dependent or independent fashions were hydrolyzed by guan-osine 5′-O-(3-thiotriphosphate) (GTPγS)- and carbachol-stimulated phospholipase C. Unlike CMP-dependent labeling, however, CMP-independent incorporation of [3H]Ins into lipids was inhibited by 1 mM (0.04%) sodium deoxy-cholate. Thus, when PtdIns labeling and phospholipase C stimulation were studied in a concerted fashion, [3H]Ins was incorporated into lipids primarily through the Ptdlns synthase-catalyzed reaction because of the presence of deoxy-cholate required to observe carbachol-stimulation of phospholipase C. Little direct breakdown of [3H]PtdIns was detected because production of myo-[3H]inositol 1-mono- phosphate was minimal and myo-[3H]inositol 1,4-bisphos-phate was the predominant product. Although PtdIns labeling and 3Hpolyphosphoinositide formation were unaffected by GTPγS and carbachol and had no or little lag period, GTPγS- and carbachol-stimulated appearance of 3H-Ins phosphates exhibited an appreciable lag (10 min). Also, flux of label from [3H]Ins to 3H-Ins phosphates was restricted to a narrow range of free calcium concentrations (10–300 nM). These results show the concerted activities of Ptdlns synthase, Ptdlns 4-kinase, and phospholipase C, and constitute a simple assay for guanine nucleotide-dependent agonist stimulation of phospholipase C in a brain membrane system using [3H]Ins as labeled precursor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10958.x
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  • 93
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    Two Forms of GO Type G Proteins: Identification and Distribution in Various Rat Tissues and Cloned Cells (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
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    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: A Go type G protein distinct from the major species of Go was recently isolated from bovine brain and designated Go*. The cDNAs encoding two forms of mammalian Goα were also isolated and designated GoAα and GoBα. To recognize two forms of Go type G proteins, we raised antibodies in rabbits against two peptides with sequences found only in the respective proteins of murine GoAα (SNTYE-DAAAYIQTQF) and GoBα (TEAVAHIQGQYESK). Purified anti-GoAα antibodies reacted with the major species of Goα purified from bovine and rat brain, whereas anti-GoBα antibodies reacted only with rat Go*α, but not with the major species of Goα or bovine Go*α. These results indicate that the major species of Goα is encoded by GoAα cDNA and Go*α is encoded by GoBα cDNA. Using these antibodies, the distribution of GoA and GoB was studied in various rat tissues and cloned cells. Both GoA and GoB were present in many tissues, but their distribution in peripheral tissues was distinct. GoAα seemed to associate mainly with neural tissues. On the other hand, relatively high concentrations of GoBα were present in the brain, pituitary gland, adipose tissue, lung, and testis. The concentrations of both GoA and GoB in the brain increased during ontogenic development, but the increase in GoB was observed at a later age. Both GoA and GoB were found in such cloned cells as PC 12, NG108-15, C6, GA-1, G8, and 3T3-L1 cells. Treatment of PC 12 cells with nerve growth factor caused the extension of neuron-like processes and the increase in the level of GoA, but not in the level of GoB.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10961.x
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  • 94
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    Changes in Aldose Reductase After Crush Injury of Normal Rat Sciatic Nerve (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
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    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The response of aldose reductase (AR) to crush injury was studied in normal rat sciatic nerve. Enzyme activity and immunoreactivity of AR were determined at intervals of 1, 5, 14, 28, and 35 days after crush and correlated with histologic and immunocytochemical observations. During nerve degeneration in the distal segments of crushed nerves, a significant reduction in AR activity was detected. At 5 and 14 days, coincident with Schwann cell proliferation, enzyme activity decreased by nearly two- and fourfold, respectively. Although activity of AR increased by 28 days during nerve regeneration, it was not restored to normal levels at 35 days. Similar reductions were observed with the immunoblotting of the enzyme. Quantitative analysis of immunogold labelling on electron micrographs confirmed that proliferating as well as remyelinating Schwann cells contained reduced gold particle density compared to Schwann cells of noncrushed myelinated fibers. Immunoblots of P0, a marker for the degree of Schwann cell differentiation or myelination, showed that the temporal sequence of changes in P0 paralleled that of AR. Thus expression of AR is a function of differentiated or mature Schwann cells. The putative volume regulatory role of AR in Schwann cells may become superfluous during Wallerian degeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10966.x
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  • 95
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    Butyrylcholinesterase from Chicken Brain Is Smaller than That from Serum: Its Purification, Glycosylation, and Membrane Association (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Applying a new four-step isolation procedure, we have purified butyrylcholinesterase (BChE) from chicken serum to homogeneity with more than 250 U/mg specific activity. The serum enzyme was used for producing monoclonal antibodies. These BChE-specific antibodies also recognize BChE from brain, and thus enabled us to isolate the enzymes from embryonic and adult brain that occur only in minute amounts. More than 50% of the brain BChE is membrane-bound. The catalytic and inhibition properties of brain BChE are similar to those of serum BChE. However on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the serum enzyme is represented by a double-band of 79/82 kDa, whereas the brain enzyme has a size of 74 kDa. Limited digestion of the serum and brain preparations by V8-protease leads to similar peptide patterns. Enzymatic deglycosylation shows that their core proteins consist of 59-kDa subunits and that the different molecular weights are due to different glycosylation patterns. The differently sized glycosylation parts of brain and serum BChE may indicate that they subserve different functions. Furthermore, the membrane-bound brain BChE can be solubilized by Pronase or protease K, but not by phosphatidylinositol-specific phospholipase C.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10969.x
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  • 96
    Electronic Resource
    Electronic Resource
    Detergent-Insoluble Cortical Lewy Body Fibrils Share Epitopes with Neurofilament and τ (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Lewy bodies are cytoskeletal inclusions associated with neuronal injury and death in idiopathic Parkinson's disease and other neurodegenerative disorders. The chemical composition of the 8–10-nm fibrils of the Lewy body is unknown, although they are related to both normal cytoskeletal elements and paired helical filaments of Alzheimer neurofibrillary tangles. From the Lewy body-rich cerebral cortex of patients with diffuse Lewy body disease we have isolated intact Lewy bodies using a high salt buffer/nonionic detergent gradient centrifugation procedure and extracted the constitutive fibrils with urea and sodium dodecyl sulfate. Urea/detergent-resistant Lewy body fibrils were solubilized with formic acid and found to contain a single protein band of 68 kDa, which was not found in identically prepared normal brain homogenates. The Lewy body derived-polypeptide was recognized on immunoblots by a polyclonal antibody that reacted with both the 68-kDa neurofilament subunit and the microtubule-associated protein τ. The 68-kDa Lewy body protein was not labeled by the monoclonal antibody τ-1 despite prior in vitro enzymatic dephosphorylation. We conclude that the detergent-insoluble component of the cortical Lewy body fibril shares epitopes with neurofilament and τ and may be a posttranslationally modified derivative of either neurofilament or τ with substantially altered biochemical and immunologic properties.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10074.x
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  • 97
    Electronic Resource
    Electronic Resource
    Release of Excitatory Amino Acids from Cultured Hippocampal Astrocytes Induced by a Hypoxic-Hypoglycemic Stimulation (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: An excess release of excitatory amino acids (EAA) is an important factor for postischemic brain damage. In the present communication, we demonstrate that cultured hippocampal cells release EAA after hypoxic-hypoglycemic treatment. The amounts of EAA released from astrocytes were appreciably above those released from neurons. Furthermore, the amount of aspartate released from astrocytes was comparable to that of glutamate, although the endogenous content of aspartate was one-fifth that of glutamate. The endogenous content of aspartate in astrocytes increased even after hypoxic-hypoglycemic treatment. These results suggests that ischemic neuronal death is due, at least in part, to the excitotoxicity of aspartate and glutamate-derived from surrounding astrocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10075.x
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  • 98
    Electronic Resource
    Electronic Resource
    Astrocyte Heterogeneity: Endogenous Amino Acid Levels and Release Evoked by Non-N-Methyl-D-Aspartate Receptor Agonists and by Potassium-Induced Swelling in Type-1 and Type-2 Astrocytes (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The aim of the present study was to determine whether endogenous amino acids are released from type-1 and type-2 astrocytes following non-N-methyl-D-aspartate (NMDA) receptor activation and whether such release is related to cell swelling. Amino acid levels and release were measured by HPLC in secondary cultures from neonatal rat cortex, highly enriched in type-1 or type-2 astrocytes. The following observations were made. (a) The endogenous level of several amino acids (glutamate, alanine, glutamine, asparagine, taurine, serine, and threonine) was substantially higher in type-1 than in type-2 astrocytes. (b) The spontaneous release of glutamine and taurine was higher in type-1 than in type-2 astrocytes; that of other amino acids was similar. (c) Exposure of type-2 astrocyte cultures to 50 μM kainate or quisqualate doubled the release of glutamate and caused a lower, but significant increase in that of aspartate, glycine, taurine, alanine, serine (only in the case of kainate), and glutamine (only in the case of quisqualate). These effects were reversed by the antagonist CNQX. (d) Exposure of type-1 astrocyte cultures to 50–200 μM kainate or 50 μM quisqualate did not affect endogenous amino acid release, even after treating the cultures with dibutyryl cyclic AMP. (e) Exposure of type-1 or type-2 astrocyte cultures to 50 mM KCl (replacing an equimolar concentration of NaCl) enhanced the release of taurine 〉 glutamate 〉 aspartate. The effect was somewhat more pronounced in type-2 than in type-1 astrocytes. Veratridine (50 μM) did not cause any increase in amino acid release. (f) The release of amino acids induced by high [K+] appeared to be related to cell swelling, in both type-1 and type-2 astrocytes. Swelling and K+-induced release were somewhat higher in type-2 than in type-1 astrocytes. In contrast, neither kainate nor quisqualate caused any appreciable increase in cell volume. It is concluded that non-NMDA receptor agonists stimulate the release of several endogenous amino acids (some of which are neuroactive) from type-2 but not from type-1 astrocytes. The effect does not seem to be related to cell swelling, which causes a different release profile in both type-1 and type-2 astrocytes. The absence of kainate- and quisqualate-evoked release in type-1 astrocytes suggests that the density of non-NMDA receptors in this cell type is very low.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10073.x
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  • 99
    Electronic Resource
    Electronic Resource
    Inhibition of Forskolin-Stimulated Cyclic AMP Formation by 1-Aminocyclopentane-trans-1,3-Dicarboxylate in Guinea-Pig Cerebral Cortical Slices (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effects of the selective metabotropic glutamate receptor agonist 1-aminocyclopentane-trans-1,3-dicarboxylate (t-ACPD) on forskolin-stimulated cyclic AMP formation in guinea-pig cerebral cortex slices were determined. t-ACPD inhibited the accumulation of [3H]cyclic AMP by ∼80%, with an IC50 value of 35 ± 4 μM. The effect was reversible and stereoselective, with the 1S,3R isomer being ∼400-fold more potent than the 1R,3S isomer. L-Glutamate (over a restricted concentration range) also partially inhibited the response to forskolin, but quisqualate, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), and N-methyl-D-aspartate (NMDA) were ineffective. The effect of t-ACPD was not blocked by antagonists of the phospholipase C-linked metabotropic glutamate receptor, the AMPA ionotropic glutamate receptor, or the NMDA receptor. In summary, our results indicate the presence of a glutamate receptor in guinea-pig brain that is activated selectively by t-ACPD and that is negatively linked to adenylyl cyclase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb10077.x
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  • 100
    Electronic Resource
    Electronic Resource
    Different Glycosylation in Acetylcholinesterases from Mammalian Brain and Erythrocytes (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Acetylcholinesterases (EC 3.1.1.7, AChE) have varying amounts of carbohydrates attached to the core protein. Sequence analysis of the known primary structures gives evidence for several asparagine-linked carbohydrates. From the differences in molecular mass determined on sodium dodecyl sulfate-polyacrylamide gel before and after deglycosylation with N-glycosidase F (EC 3.2.2.18), it is seen that dimeric AChE from red cell membranes is more heavily glycosylated than the tetrameric brain enzyme. Furthermore, dimeric and tetrameric forms of bovine AChE are more heavily glycosylated than the corresponding human enzymes. Monoclonal antibodies 2E6, 1H11, and 2G8 raised against detergent-soluble AChE from electric organs of Torpedo nacline timilei as well as Elec-39 raised against AChE from Electrophorus electricus cross-reacted with AChE from bovine and human brain but not with AChE from erythrocytes. Treatment of the enzyme with N-glycosidase F abolished binding of monoclonal antibodies, suggesting that the epitope, or part of it, consists of N-linked carbohydrates. Analysis of N-acetylglucosamine sugars revealed the presence of N-acetylglucosamine in all forms of cholinesterases investigated, giving evidence for N-linked glycosylation. On the other hand, N-acetylgalactosamine was not found in AChE from human and bovine brain or in butyrylcholinesterase (EC 3.1.1.8) from human serum, indicating that these forms of cholinesterase did not contain O-linked carbohydrates. Despite the notion that within one species, the different forms of AChE arise from one gene by different splicing, our present results show that dimeric erythrocyte and tetrameric brain AChE must undergo different postsynthetic modifications leading to differences in their glycosylation patterns.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11333.x
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