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  • 1985-1989  (641,265)
  • 1980-1984  (515,399)
  • 1975-1979  (465,514)
Source
Material
Years
Year
Person/Organisation
Keywords
Language
  • 1
    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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  • 2
    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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  • 3
    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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  • 4
    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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  • 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
    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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  • 7
    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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  • 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
    ¬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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  • 11
    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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  • 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
    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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  • 14
    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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  • 15
    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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  • 16
    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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  • 17
    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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  • 18
    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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  • 19
    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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  • 20
    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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  • 21
    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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  • 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
    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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  • 24
    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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  • 25
    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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  • 26
    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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  • 27
    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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  • 28
    Journal/Serial
    Journal/Serial
    Informationstechnik : it ; Computer, Systeme, Anwendungen (from 1986-1992)
    München :Oldenbourg, ; 28.1986 - 34.1992
    Details
    Title: Informationstechnik : it ; Computer, Systeme, Anwendungen
    Publisher: München :Oldenbourg,
    Year of publication: 1986-1992
    Dates of Publication: 28.1986 - 34.1992
    ISSN: 0179-9738 , 0013-5720
    Type of Medium: Journal/Serial
    Language: Undetermined
    Former Title: Vorg. ---〉:Elektronische Rechenanlagen
    Subsequent Title: Forts. ---〉:Informationstechnik und technische Informatik
    Note: it-Seminar
    Additional Information: Beil. ---〉:Euro-KI-Führer
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  • 29
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    Journal/Serial
    SIGACT news : publ. by the ACM Special Interest Group on Automata and Computability Theory (from 1969-1992)
    New York, NY :ACM, ; 1.1969 - 23.1992,2 = Nr. 1-83
    Details
    Title: SIGACT news : publ. by the ACM Special Interest Group on Automata and Computability Theory
    Author: Association for Computing Machinery / Special Interest Group on Automata and Computability Theory
    Contributer: Association for Computing Machinery / Special Interest Committee on Automata and Computability Theory
    Publisher: New York, NY :ACM,
    Year of publication: 1969-1992
    Dates of Publication: 1.1969 - 23.1992,2 = Nr. 1-83
    ISSN: 0163-5700
    Type of Medium: Journal/Serial
    Subsequent Title: Forts. ---〉:Association for Computing Machinery / Special Interest Group on Algorithms and Computation Theory: SIGACT news
    Additional Information: In 12.1980,2 Index 1/12.1969/80 von ---〉:Symposium on Theory of Computing: Conference record of the ... annual ACM Symposium on Theory of Computing
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  • 30
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    Journal/Serial
    Soviet journal of numerical analysis and mathematical modelling (from 1986-1991)
    Utrecht :VNU Science Press, ; 1.1986 - 6.1991
    Details
    Title: Soviet journal of numerical analysis and mathematical modelling
    Publisher: Utrecht :VNU Science Press,
    Year of publication: 1986-1991
    Dates of Publication: 1.1986 - 6.1991
    ISSN: 0169-2895
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: Forts. ---〉:Russian journal of numerical analysis and mathematical modelling
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  • 31
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    Journal/Serial
    SIGPLAN notices : a monthly publication of the Special Interest Group on Programming Languages of the Association for Computing Machinery (from 1966-1991)
    New York, NY :ACM, ; 1.1966 - 26.1991,9u.11
    Details
    Title: SIGPLAN notices : a monthly publication of the Special Interest Group on Programming Languages of the Association for Computing Machinery
    Author: Association for Computing Machinery / Special Interest Group on Programming Languages
    Publisher: New York, NY :ACM,
    Year of publication: 1966-1991
    Dates of Publication: 1.1966 - 26.1991,9u.11
    ISSN: 0362-1340
    Type of Medium: Journal/Serial
    Language: Undetermined
    Subsequent Title: 26.1991,10 u. Forts. ---〉:Association for Computing Machinery / Special Interest Group on Programming Languages: ACM SIGPLAN notices
    Additional Information: 6,2=1971 von:Symposium on Data Structures in Programming Languages: Proceedings of a Symposium on Data Structures in Programming Languages
    Additional Information: 17,4=10,2; 22,10=15,5; 24,spec.iss.=17,2; 26,4=19,2 von:Computer architecture news
    Additional Information: 21,10=1986 von:Workshop on Object Oriented Programming: Transcript
    Additional Information: 11,6=10,1 von:Computer graphics
    Additional Information: 16,6=2,1/2 von:Association for Computing Machinery / Special Interest Group on Office Automation: SIGOA newsletter
    Additional Information: 14,8=1979; 17,6=1982; 19,6=1984; 21,7=1986 von:Symposium on Compiler Construction: Proceedings of the SIGPLAN Symposium on Compiler Construction
    Additional Information: 20,7=1985 von:Symposium on Language Issues in Programming Environments: Proceedings of the ACM SIGPLAN ... Symposium on Language Issues in Programming Environments
    Additional Information: 19,5=1; 22,1=2; 24,2=3 von:Software Engineering Symposium on Practical Software Development Environments: Proceedings of the ACM SIGSOFT SIGPLAN Software Engineering Symposium on Practical Software Development Environments
    Additional Information: 22,10=2; 24,spec.iss.=3 von:International Conference on Architectural Support for Programming Languages and Operating Systems: Proceedings
    Additional Information: 23,7=1988; 24,7=1989; 25,6=1990 von:Conference on Programming Language Design and Implementation: Proceedings of the SIGPLAN ... Conference on Programming Language Design and Implementation
    Additional Information: 21,11=1; 22,12=2; 23,11=3; 24,10=4 von:OOPSLA: Conference proceedings
    Additional Information: 22,10=21,4; 24,spec.iss.=23,spec.iss.; 26,4=25,spec.iss. von:Operating systems review
    Additional Information: 17,4=1982 von:Symposium on Architectural Support for Programming Languages and Operating Systems: Proceedings
    URL: 5.1970 - 34.1999: Contents; 35.2000 -: Volltexte
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  • 32
    Electronic Resource
    Electronic Resource
    Mitochondrial and Peroxisomal β-Oxidation of Stearic and Lignoceric Acids by Rat Brain (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Crude subcellular fractions were prepared from adult rat brains by differential centrifugation of brain ho-mogenates. Greater than 98% of the cellular mitochondrial marker enzyme activity sedimented in the heavy and light mitochondrial pellets, and 〈1% of the activity sedimented in microsomal pellets. Lysosomal marker enzyme activities mainly (71-78% of cellular activity) sedimented in the heavy and light mitochondrial pellets. Significant amounts of the lysosomal marker enzyme activity also sedimented in the crude microsomal pellets (9-13% of total) and high-speed supernatants (14-16% of total). The specific activities of microsomal and peroxisomal marker enzyme activities were highest in the crude microsomal pellets. Fractionation of the crude microsomal pellets on Nycodenz gradients resulted in the separation of the bulk of the remaining mitochondrial, lysosomal, and microsomal enzyme activities from peroxisomes. Fatty acyl-CoA synthetase activities separated on Nycodenz gradients as two distinct peaks, and the minor peak of the activities was in the peroxisomal enriched fraction. Fatty acid β-oxidation activities also separated as two distinct peaks, and the activities were highest in the peroxisomal enriched fractions. Mitochondria were purified from the heavy mitochondrial pellets by Percoll density gradients. Fatty acyl-CoA synthetase and fatty acid β-oxidation activities were present in both the purified mitochondrial and peroxisomal enriched fractions. Stearoyl-CoA synthetase activities were severalfold greater compared to lignoceroyl-CoA synthetase, and stearic acid β-oxidation was severalfold greater compared to lignoceric acid β-oxidation in purified mitochondrial and peroxisomal enriched fractions. The results presented demonstrate conclusively that, in contrast to rat liver and human skin fibroblasts, rat brain mitochondria contain lignoceroyl-CoA synthetase, as well as lignoceric acid β-oxidation activities
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09235.x
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  • 33
    Electronic Resource
    Electronic Resource
    Properties of a Protein Kinase C Activity in Synaptic Plasma Membrane and Postsynaptic Density Fractions Isolated from Canine Cerebral Cortex (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Protein kinase C (PKC) activity (phosphorylation increased by addition of Ca2+/phosphatidylserine or Ca2+/ phosphatidylserine/phorbol ester) was found in both a synaptic plasma membrane (SPM) and a postsynaptic density (PSD) fraction. The SPM fraction had as endogenous substrates 87K-, 60K-, 50K-, and 20K-Mr proteins, whereas the PSD fraction had only the 20K-Mr protein. The PKC activity was also detected using histone III-S as a substrate, in SPM but much less in PSD. Phosphorylations of histone and the endogenous substrates of PKC, assayed in the absence of Ca2+, were enhanced in the SPM prepared after treatment of brain homogenate with phorbol 12-myristate 13-acetate (TPA), but very little enhancement was found in PSD after such treatment. The SPM PKC activity (both for endogenous substrate proteins and for histone), which was enhanced by TPA treatment of brain homogenate, was inhibited by calcium (IC50, 3 × 10−7M). The phosphorylations of the 20K-Mr protein in PSD, and in SPM prepared with and without TPA treatment, were all inhibited by H-7. The 20K-Mr protein in the PSD fraction is also phosphorylated by a PSD Ca2+/calmodulin-dependent protein kinase II. The evidence indicates that both SPM and PSD fractions contain a PKC activity. Detergent treatment of SPM, to produce a purified PSD fraction, results in a PSD fraction that has lost most of the endogenous substrates, lost the TPA-induced enhanced activity assayed in the absence of Ca2+, and lost the inhibitory effect of low Ca2+ concentration
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09240.x
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  • 34
    Electronic Resource
    Electronic Resource
    Adrenergic Receptors in Aging and Alzheimer's Disease: Increased β2-Receptors in Prefrontal Cortex and Hippocampus (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Loss of pigmented noradrenergic locus ceruleus neurons occurs in Alzheimer's disease (AD) and, to a lesser extent, in aging. We studied β-adrenergic receptors and their subtypes, β1 and β2, by the specific binding of 125I-pindolol to particulate membrane preparations from prefrontal cortex, hippocampus, putamen, and cerebellum and to sections from frontal cortex by in vitro autoradiography. In prefrontal cortex from controls, numbers of total β- and β-adrenoceptors did not significantly correlate with age, but number of β1-adrenoceptors showed a weak but significant negative correlation. Binding in tissue particulate preparations to total β-receptors did not reveal significant differences in samples from prefrontal cortex between AD subjects and age-matched controls. However, β1-adrenoceptors were decreased and β2-adrenoceptors were increased in number by ∼30-50% in AD subjects. Thus, the relative ratio of β/β2-receptors was decreased in AD. Binding by in vitro receptor autoradiography performed in a subset of samples of frontal cortex also showed β2-adrenoceptors, and less consistently total β-and β1recep-tors, to be increased significantly in number in cortical laminae II, III, IV, and V of tissue sections from AD subjects. In these subjects, number of locus ceruleus cells and norepinephrine concentrations in putamen and frontal cortex were markedly reduced compared with values in controls. In the hippocampus, total β- and both β2- and β1-adrenoceptors were increased in number in AD. In contrast, in the putamen. where β-receptors predominate, total β- and β1-receptors were significantly decreased in number with no consistent change in content of β2-receptors in AD. There were no significant changes in the cerebellum. Specific pindolol binding was not affected by interval between death and sampling of tissue at autopsy. Our results indicate selective changes in number of β-receptors in AD. These changes in the cortex and hippocampus suggest receptor upregulation in response to noradrenergic deafferentation from the locus ceruleus or may simply reflect glial proliferation in AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09242.x
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  • 35
    Electronic Resource
    Electronic Resource
    A Kainate Receptor Linked to Nitric Oxide Synthesis from Arginine (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In slices of young rat cerebellum, the glutamate analogue kainate induced a large accumulation of cyclic GMP, which was inhibited by non-TV-methyl-D-aspartate antagonists. Quisqualate and a-amino-3-hydroxy-5-methyl-4-isoxazoIepropionate evoked only small cyclic GMP responses and inhibited the effect of kainate. When tested in cerebellar cell suspensions, glutamate was also a potent antagonist of the cyclic GMP response to kainate. Superoxide dismutase enhanced the response in the isolated cells, whereas haemoglobin and methylene blue were inhibitory. The response in slices was Ca2+ dependent, augmented by arginine, and inhibited by l-NG-mono-methylarginine in a manner that could be reversed by additional arginine. It is concluded that stimulation of kainate receptors leads to activation of the enzyme that synthesises nitric oxide from arginine and that activation of soluble guanylate cyclase by the released nitric oxide accounts for the cyclic GMP generation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09266.x
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  • 36
    Electronic Resource
    Electronic Resource
    Brief Instructions to Authors (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), 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.1471-4159.1989.tb09269.x
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  • 37
    Electronic Resource
    Electronic Resource
    Calendar of Events (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), 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.1471-4159.1989.tb09271.x
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  • 38
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    Electronic Resource
    Kinetic Analysis of Leucine-Enkephalin Cellular Uptake at the Luminal Side of the Blood-Brain Barrier of an In Situ Perfused Guinea-Pig Brain (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The uptake of enkephalin-(5-L-leucine) (Leu-en-kephalin) at the luminal side of the blood-brain barrier was measured by means of an in situ vascular brain perfusion technique in the anaesthetized guinea pig. This method allows measurements of cerebrovascular peptide uptake over periods of up to 20 min, and excludes the solute under study from the general circulation and systemic metabolic influences. A capillary unidirectional transfer constant, Kin, for [tyrosyl-3,5-3H]Leu-enkephalin was estimated graphically from the multiple-time brain uptake data in the presence of different concentrations of unlabelled peptide, and dose-dependent self-inhibition was demonstrated. Analysis of unidirectional influx of blood-borne Leu-en kephalin into the brain revealed Michaelis-Menten saturation kinetics in the parietal cortex, caudate nucleus, and hippocampus, with Vmax between 0.14 and 0.16 nmol min−1 g−1 and Km ranging from 34 to 41 μM, for the saturable component, whereas the estimated diffusion constant, Kd, was not significantly different from zero. Entry of [3H]Leu-enkephalin was not inhibited in the presence of either a 5 mM concentration of unlabelled L-tyrosine, tyro-sylglycine, and tyrosylglycylglycine, or aminopeptidase inhibitor, bestatin (0.5 mM), suggesting that the saturable mechanism of the tracer at the luminal side of the blood-brain barrier does not involve uptake of the peptide's N-terminal amino acid and/or its tyrosine-containing fragments. The specific δ-opioid antagonist, allyl2-Tyr-AIB-Phe-OH, and μ-opioid receptor agonist, Tyr-D-Ala-Gly-Me-Phe-NH(CH2)20H, at concentrations in the perfusate above the Km value for the saturable transport of Leu-enkephalin, did not affect significantly uptake of [3H]Leu-enkephalin. The present study provides, for the first time, a characterization of the kinetic parameters of the unidirectional uptake of a peptide from the luminal side of the blood-brain barrier
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08522.x
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  • 39
    Electronic Resource
    Electronic Resource
    Bovine Brain Endothelial Cells Express Tight Junctions and Monoamine Oxidase Activity in Long-Term Culture (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The passage of substances across the blood-brain barrier is regulated by cerebral capillaries which possess certain distinctly different morphological and enzymatic properties compared to capillaries of other organs. Investigations of the functional characteristics of brain capillaries have been facilitated by the use of cultured brain endothelial cells, but in most studies a number of characteristics of the in vivo system are lost. To provide an in vitro system for studies of brain capillary functions, we developed a method of isolating and producing a large number of bovine brain capillary endothelial cells. These cells, absolutely free of pericyte contamination, are subcultured, at the split ratio of 1:20 (20-fold increase of the cultured surface), with no apparent changes in cell morphology up to the fiftieth generation (10 passages). Retention of endothelial-specific characteristics (factor V11I-related antigen, angiotensin-converting enzyme, and nonthrombogenic surface) is shown for brain capillary-derived endothelial cells up to passage 10, even after frozen storage at passage 3. Furthermore, we showed that bovine brain capillary endothelial cells retain, up to the fiftieth generation, some of the characteristics of the blood-brain barrier: occurrence of tight junctions, paucity of pinocytotic vesicles, and monoamine oxidase activity
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08526.x
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  • 40
    Electronic Resource
    Electronic Resource
    [3H]GBR 12935 Binding to Dopamine Uptake Sites in the Human Brain (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Binding of l-[2-(diphenylmethoxy)ethyl]-4-(3-phenylpropyl)piperazine ([3H]GBR 12935) was studied in membrane preparations of several human brain regions. In putamen, the substituted piperazine derivates cis- and trans-flupenthixol displaced 90% of the total [3H]GBR 12935 binding. Computer-assisted analysis of the competition curves revealed a high-affinity site (30%; KiH= 54 μM) and a low-affinity site (60%; KiL= 4.5 μM). The dopamine uptake blockers mazindol and nomifensine only displaced 30% of the total [3H]GBR 12935 binding in a monophasic way. Binding of [3H]GBR 12935 to the dopamine uptake sites, i.e., that displaced by dopamine uptake blockers, corresponded to part of the binding having low affinity for flupen-thixol and was only detected in putamen, nucleus caudatus, nucleus accumbens, and substantia nigra. Even after masking the high-affinity binding site for flupenthixol by including 1 μM cis-flupenthixol in the binding assays, no dopamine uptake sites could be detected in globus pallidus, amygdala, thalamus, hippocampus, and cerebral cortex. Binding of [3H]GBR 12935 to dopamine uptake sites was lost in the nucleus caudatus ipsilateral to ventral midbrain infarctions, confirming their location on nigrostriatal nerve endings. Gross unilateral lesions of the striato- and pallidonigral pathways did not affect the number of dopamine uptake sites in the ipsilateral substantia nigra, suggesting that they may reside on the soma or dendrites of nigral neurons
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08530.x
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  • 41
    Electronic Resource
    Electronic Resource
    Epidermal Growth Factor Enhances the Expression of an Endogenous Lectin in Aggregating Fetal Brain Cell Cultures (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Aggregating cell cultures prepared from fetal rat telencephalon express the two subunits [cerebellar soluble lectins (CSL) 1 and 2] of a soluble, mannose-specific endogenous lectin (CSL) in a development-dependent manner. Increased CSL synthesis was found at an early postmitotic stage as well as during the period of maximal myelination. Repet-tive treatment of early cultures with epidermal growth factor EGF, 3 nM) caused a great stimulation of CSL biosynthesis. Immunocytochemical studies revealed particularly intense CSL-specific staining in small, EGF-responsive cells, presumably glial cells. Large quantities of CSL-immunoreactive material were found also in the extracellular space and on the external side of the plasma membrane, indicating abundant release of CSL. The present findings suggest that EGF or EGF-related factors in the brain are able to regulate the expression of an endogenous lectin, affecting brain ontogeny.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08535.x
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  • 42
    Electronic Resource
    Electronic Resource
    Comparison of the Effects of Ions and GTP on Substance P Binding to Membrane-Bound and Solubilized Specific Sites (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Mg2+ increased but Na+ and GTP decreased [3H]substance P (SP) binding to rat cerebral cortical membranes and to 10 mM 3-[(3-cholamidopropyl)dimethyl-ammonio]-l-propane sulfonate (CHAPS)-solubilized membrane fraction. To determine the binding parameters that are modified by the cations and GTP, inhibition experiments of [3H]SP binding by unlabeled SP were performed in both of the preparations. Nonlinear least-squares regression analysis of data in the membrane fraction indicated that optimal fitting of the inhibition curves in the presence of 10 mM MgCl2 was attained with a two-site model, corresponding to a “high-affinity (H)” and a “low-affinity (L)” state. By omitting MgCl2, or by addition of NaCl and GTP, the [3H]SP specific binding was decreased, the H state disappeared, and the L state and a new “super-low affinity (SL)” state were observed. The SP/ [3HJSP inhibition curves in the cerebral cortical membranes by in vivo treatment with pertussis toxin (islet-activating protein) were similar to that in the presence of GTP in control membranes. The effects of MgC12, NaCl, and GTP were greater in the CHAPS-solubilized fraction than in the membrane fraction. In contrast to the membrane fraction, the inhibition curves of [3HJSP binding by unlabeled SP in the presence of MgCl2 in the CHAPS-solubilized fraction were best fitted to a one-site model. The KD value was relatively close to that of the low-affinity state in the membrane fraction. Even with the addition of NaCl or GTP, or by reducing MgCI2concentration to 1 mM, although the inhibition curves consistently fit the one-site model, the KD values changed only slightly.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08534.x
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  • 43
    Electronic Resource
    Electronic Resource
    Carrier-Mediated Transport of Thyroid Hormones into Rat Glial Cells in Primary Culture (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The uptake of 3,3′,5-[3′-125I]triiodo-L-thyronine ([125I]L-T3) and of L-[3′,5′-125I]thyroxine ([125I]L-T4) by cultured rat glial cells was studied under initial velocity (Vi) conditions. Uptake of both hormones was carrier mediated and obeyed simple Michaelis-Menten kinetics. The following respective values of Km (μM) and Vmax (fmol/min/μg of DNA) were obtained at 25°C: 0.52 ± 0.09 and 727 ± 55 for L-T3 and 1.02 ± 0.21 and 690 ± 85 for L-T4. Ki values (μM) for the inhibition of [125I]L-T3 uptake by unlabeled analogues were as follows: L-T4, 0.88; 3,3′,5′-triiodo-L-thyronine, 1.4; 3,3′-diiodo-L-thyronine, 2.9; 3,3′,5-triiodo-D-thyronine, 4.8; and triiodothyroacetic acid, 5.3. These values indicate that the uptake system is stereospecific. Unlabeled L-T3 was a better competitor than unlabeled L-T4 for the uptake of [l25l]L-T4, an observation suggesting that both hormones were taken up by a common carrier system. L-T3 and L-T4 uptake was pH dependent, a finding suggesting that the phenolic unionized form of the hormones was preferentially taken up. L-T3 uptake was studied in the presence of various inhibitors; the results suggest that uptake was independent of the transmembrane Na+ gradient and of the cellular energy. Compounds that inhibited cellular uptake but were without effect on L-T3 binding to isolated nuclei also inhibited L-T3 nuclear binding in intact cells, an observation suggesting that uptake could be rate limiting for the access of L-T3 to nuclear receptors when transport is severely inhibited.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08538.x
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  • 44
    Electronic Resource
    Electronic Resource
    Muscarinic Receptor-Stimulated Phosphoinositide Turnover in Human SK-N-SH Neuroblastoma Cells: Differential Inhibition by Agents that Elevate Cyclic AMP (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The possibility that an increased intracellular concentration of cyclic AMP (cAMP) can regulate the extent of muscarinic receptor-stimulated phosphoinositide (PPI) turnover in the human neuroblastoma cell line SK-N-SH was examined. Addition of either forskolin (or its water-soluble nalog, L-85,8051), theophylline, isobutylmethylxanthine, or Liolera toxin, agents that interact with either the catalytic unit of adenylate cyclase, cAMP phosphodiesterase, or the guanine nucleotide binding protein linked to adenylate cyclase activation, resulted in a 45–181% increase in cAMP concentration and a 27–70% inhibition of carbachol-stimu-lated inositol phosphate release. Through the use of digitonin-permeabilized cells, the site of inhibition was localized to a step at, or distal to, the guanine nucleotide binding protein that regulates phospholipase C activity. In contrast, when intact SK-N-SH cells were exposed to prostaglandin E1, the ensuing increases in cAMP were not accompanied by an inhibition of stimulated PPI turnover. These differential effects of increased cAMP concentrations on stimulated PPI turnover may reflect the compartmentation of cAMP within SK-N-SH cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08541.x
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  • 45
    Electronic Resource
    Electronic Resource
    Chronic Exposure of NG 108-15 Cells to Opiate Agonists Does Not Alter the Amount of the Guanine Nucleotide-Binding Proteins Gi and GO (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We have characterized the pertussis toxin substrate in NG 108–15 cell membranes using site-specific antisera and ADP-ribosylation. Cell membranes contain two pertussis toxin-sensitive guanine nucleotide-binding protein α-subunits (Gα) whose Rf values in gel electrophoresis coincide with those of Gαo and Gαi2. The total quantity of Gi and Go im-munoreactivity amounted to 24.3 ± 2.8 pmol/mg, whereas only 1.5 ± 0.2 pmol/mg are capable of undergoing ADP-ribosylation catalyzed by pertussis toxin. Pretreatment of cells with the agonist [D-Ala2,D-Leu2]-enkephalin (DADLE) for 24 h and DADLE or morphine for 72 h did not alter the incorporation of ADP-ribose or the immunoreactive amount of Gi and Go subunits. However, pretreatment for 72 h with naloxone increased the incorporation of ADP-ribose without an apparent change in affinity or in the immunochemically determined protein levels of Gi and Go. This indicates that the process of down-regulation and desensitization of the γ-opioid receptor neither requires quantitative alterations in the levels of Gi and Go nor changes in the degree of coupling among their subunits. In contrast, chronic exposure to antagonists seems to alter the degree of precoupling between α-and β-subunits of Gi and/or Go.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08544.x
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  • 46
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    A Comparison of the Distribution of Neurotransmitters in Brain Regions of the Rat and Guinea-Pig Using a Chemiluminescent Method and HPLC with Electrochemical Detection (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Six brain areas of rats and guinea-pigs, killed by microwave irradiation, were used for the concomitant measurement of the levels and regional distribution of cholinergic, biogenic amine, and amino acid neurotransmitters and metabolites. Acetylcholine (ACh) and choline (Ch) were quantified by chemiluminescence; noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT), and their metabolites by HPLC with electrochemical detection (HPLC-EC); and six putative amino acid neurotransmitters by HPLC-EC following derivatisation. The levels and regional distribution of these transmitters and their metabolites in the rat were similar to those reported in previous studies, except that biogenic amine transmitter levels were higher and metabolite concentrations were lower. The guinea-pig showed a similar regional distribution, but the absolute levels of ACh were lower in striatum and higher in hippocampus, midbrain-hypothalamus, and medulla-pons. In all areas, the levels of Ch were higher and those of NA, 5-HT, and taurine were lower than in the rat. The most marked differences between the rat and guinea-pig were in the relative proportion of DA metabolites and 5-HT turnover, as estimated by metabolite/transmitter ratios. This study can be used as a basis for a comprehensive understanding of the central effects of drugs on the major neurotransmitter systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08547.x
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  • 47
    Electronic Resource
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    Brain Phospholipase A2 Is Activated After Experimental Closed Head Injury in the Rat (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Head injury was induced in rats by a weight drop device, falling over the left hemisphere. The rats were killed at 15 min, 4 h, and 24 h after injury. Cortical slices were taken from the injured zone, from the corresponding region of the contralateral hemisphere, and from the frontal lobe of both hemispheres. These cortical slices were incubated in the presence of a fluorescent phospholipid analogue, l-acyl-2-(N-4-nitrobenzo-2-oxa-I,3-diazole)aminocaproylphos-phatidylcholine (C6-NBD-PC) which is a substrate for phospholipase A2 (PLA2) in intact cells. The interaction of this substrate with cells produces only one fluorescent product, the fatty acid C6-NBD-FA, released from the 2-position of C6-NBD-PC. Thus, the level of C6-NBD-FA produced is a direct measure of PLA2 activity. Fifteen minutes after trauma, a 75% increase of PLA2 activity was found in the injured zone. At 4 h, the frontal lobe of the contused, left hemisphere had elevated PLA2 activity, as well as the injured zone (92 and 81%, respectively). At 24 h, PLA2 activity at the site of injury was 245% of sham. In the right, noninjured zone, no significant changes in PLA2 activity were noticed during the entire time course of the experiment. Prostaglandin E2 (PGE2) was extracted from the same cortical slices as those used for PLA2 activity measurement. A significant correlation (Pearson coefficient test, correlation coefficient = 0.469, p 〈 0.05, n = 21) was found between the elevation of PLA2 activity and PGE2 levels measured in the injured hemisphere, at 4 and 24 h. The elevation of PGE2 production induced by the trauma was abolished when the rats were pretreated with dextran 70,000, which has been previously shown to inhibit PLA2 activity. The results of this study support the hypothesis that activation of brain PLA2 is involved in the increased cerebral production of eicosanoids induced by trauma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08550.x
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  • 48
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    Production of Hyperalgesic Prostaglandins by Sympathetic Postganglionic Neurons (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Prostaglandin E2 and prostacyclin (prostaglandin 12) produce hyperalgesia in animals and humans. Because there is evidence that prostaglandins contribute to pain maintained by sympathetic nervous system activity, we evaluated whether sympathetic postganglionic neurons synthesize these hyperalgesic prostaglandins, and whether production of prostaglandins by these neurons can contribute to sensitization of primary afferent nociceptors. Intradermal injection of arachidonic acid but not linoleic acid, in the rat hindpaw, produces a decrease in mechanical nociceptive threshold. This hyperalgesic effect is prevented by indomethacin, an inhibitor of prostaglandin synthesis or by prior surgical removal of the lumbar sympathetic chain. To test the hypothesis that sympathetic postganglionic neurons are the source of prostaglandins, we measured production of prostaglandin E2 and 6-keto-prostaglandin Flα (the stable metabolite of prostacyclin) by homogenates of adult rat sympathetic postganglionic neurons from superior cervical ganglia. These homogenates produced significant amounts of prostaglandin E2 and 6-keto-prostaglandin F1α, and most of this production is eliminated by neonatal administration of 6-hydroxydopamine which selectively destroys sympathetic postganglionic neurons. These results demonstrate that sympathetic postganglionic neurons produce prostaglandins, and supports further the hypothesis that the release of prostaglandins from sympathetic postganglionic neurons contributes to the hyperalgesia associated with sympathetically maintained pain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb08557.x
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  • 49
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    Capsaicin-Induced Ion Fluxes Increase Cyclic GMP but Not Cyclic AMP Levels in Rat Sensory Neurones in Culture (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Capsaicin, which induces fluxes of sodilim, calcium, and potassium ions in a subset of both neonatal and adult rat dorsal root ganglion neurones, increased cyclic GMP (cGMP) levels by a factor of 20 (EC50 0.07 μ) to 10-20 pmol cGMP/mg protein in these cells. Cyclic AMP (CAMP) levels were unaffected. Nonneuronal cells derived from rat ganglia, and both neurones and nonneuronal cells from chick were unresponsive to capsaicin. Capsaicin-induced cGMP elevation in rat dorsal root ganglion (DRG) neurones was unaffected by pertussis toxin, lowered by compounds that block voltage-sensitive calcium channels, and was abolished by the removal of extracellular calcium. Calcium, guanidine, and rubidium fluxes were unaffected by treatment of DRG cells with sodium nitroprusside or dibutyryl cGMP. The cGMP response to capsaicin is thus a function of capsaicin-evoked calcium uptake through voltage-sensitive calcium channels. Elevated cGMP levels do not, however, contribute to capsaicin-evoked ion fluxes or to their desensitisation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07416.x
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  • 50
    Electronic Resource
    Electronic Resource
    Actions of Excitatory Amino Acids on Somatostatin Release from Cortical Neurons in Primary Cultures (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: L-Glutamate, N-methyl-D-aspartic acid (NMDA), quisqualate, and kainate were found to increase endogenous somatostatin release from primary cultures of rat cortical neurons in a dose-dependent manner. The rank order of potency calculated from the dose-response curves was quisqualate 〉 glutamate = NMDA 〉 kainate, with EC50 values of 0.4, 20, and 40 μM, respectively. Alanine, glutamine, and glycine did not modify the release of somatostatin. The stimulation of somatostatin release elicited by L-glutamate was Ca2+ dependent, was decreased by Mg2+, and was blocked by DL-amino-5-phosphonovaleric acid (APV) and thienyl-phencyclidine (TCP), two specific antagonists of NMDA receptors. The NMDA stimulatory effect was strongly inhibited by APV in a competitive manner (IC50= 50 μM) and by TCP in a noncompetitive manner (IC50= 90 nM). The release of somatostatin induced by the excitatory amino acid agonists was not blocked by tetrodotoxin (1 μM), a result suggesting that tetrodotoxin-sensitive, sodium-dependent action potentials are not involved in the effect. Somatostatin release in response to NMDA was potentiated by glycine, but the inhibitory strychnine-sensitive glycine receptor did not appear to be involved. Our data suggest that glutamate exerts its stimulatory action on somatostatin release essentially through an NMDA receptor subtype.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07406.x
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  • 51
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    The Novel Neuropsychotropic Agent Milacemide Is a Specific Enzyme-Activated Inhibitor of Brain Monoamine Oxidase B (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The novel neuropsychotropic agent milacemide hydrochloride (2-n-pentylaminoacetamide HCl) is a highly selective substrate of the B form of monoamine oxidase (EC 1.4.3.4; MAO). Under the in vitro conditions used in the present study, milacemide acts as an enzyme-activated, par-tially reversible inhibitor of MAO-B. A reversible inhibition of MAO-A activity is also observed at high concentrations. The inhibitory activity of milacemide is significantly greater for MAO-B. In vivo, after single or repeated oral administration, a specific inhibition of MAO-B is apparent in brain and liver, with a lack of inhibition of the MAO-A Activity. In contrast to the irreversible inhibitory action of L-deprenyl, the recovery of MAO-B activity in vivo after milacemide administration is significantly faster, a result suggesting that it is a partially reversible inhibitor. The selective inhibitory effect of milacemide for MAO-B in vivo is confirmed by its potentiation of phenylethylamine-induced stereotyped behavior, whereas vasopressor responses to tyramine were not affected. These observations suggest that milacemide could enhance dopaminergic activity in the brain and could be used as therapy for Parkinson's disease in association with L-3,4-dihydroxyphenylalanine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07403.x
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  • 52
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    Characterization and Regional Distribution of Peptides Derived from the Vasoactive Intestinal Peptide Precursor in the Normal Human Brain (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: To study the biosynthetic processing of the precursor for vasoactive intestinal peptide (prepro-VIP) in the human brain, we have developed antiseraj against the five functional domains of the precursor molecule: prepro-VIP 22-79, peptide histidine methionine (PHM), prepro-VIP 111-122, VIP, and prepro-VIP 156-170. The antisera were used in radioimmunoassays in combinatioin with HPLC to identify and quantify the peptides in regions of the human brain. All five peptides were expressed, but mainly in non-equimolar ratios. In only three regions were the same amounts of VIP and PHM found; in the remaining areas the concentration of PHM was two-thirds that of VIP. The concentrations of prepro-VIP 22-79, prepro-VIP 111-122, and prepro-VIP 156-170 were considerably lower than the corresponding VIP concentrations, and the relative concentration of prepro-VIP 111-122 differed between cortical and subcortical areas. A small proportion of the VIP precursor followed a pathway in which the dibasic conversion site after PHM is not cleaved, as evidenced by the presence of a C-terminally extended form of PHM. Finally, it was found that the C-terminal lysine residue of prepro-VIP is not removed during processing. The findings indicate that differences in the posttranslational processing of prepro-VIP exist in subpopulations of neurons in the human brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07407.x
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  • 53
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    Allosteric Activation off Brain Mitochondrial Ca2+ Uptake by Spermine and by Ca2+: Developmental Changes (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Kinetic analysis of 45Ca2+ uptake by raj brain mitochondria in Ca2+-l,2-bis(o-aminophenoxy)ethane-N, N,N′.N′-tetraacetic acid buffers indicated that spermine both increased the apparent affinity for Ca2+ and decreased the cooperativity of uptake. Both effects are consistent with an allosteric activation of uptake by spermine. The stimulating effect of spermine on 45Ca2+ uptake was maximal with mitochondria from postnatal day 10 animals and then steadily decreased with increasing age to reach adult values by ∼30 postnatal days; this was observed independently of the substrates used to fuel mitochondria. Mitochondrial Ca2+ buffering was also analyzed by use of a Ca2+-selective electrode. Addition of a large bolus of Ca2+ produced a decrease in the subsequent equilibrium extramitochondrial Ca2+ concentration (or a “rebound overshoot”) under some conditions. It is proposed that this effect is the result of an allosteric activation of Ca2+ uptake by Ca2+. This effect was slowly reversible, or hysteretic, and was blocked by spermine. The overshoot was increased in the presence of higher concentrations of Mg2+ and was absent when mitochondria were incubated with 0.3 mM Mg2+. It was maximal in mitochondria prepared from early postnatal brain, and changes in the magnitude of the effect during development paralleled those obtained with spermine stimulation of 45Ca2+ uptake. The data suggest that spermine produces an allosteric activation of Ca2+ uptake by binding to the same regulatory sites that are involved in the Ca2+-induced activation. The results as a whole suggest that spermine could modulate mitochondrial buffering of the intracellular Ca2+ concentration in brain, particularly during the early postnatal period.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07411.x
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  • 54
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    Modulation of Tryptophan Hydroxylase Activity by Phospholipids: Stimulation Followed by Inactivation (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The activity of tryptophan hydroxylase from the rat brainstem was stimulated rapidly three- to fourfold by the addition of phosphatidylinositol or phosphatidylserine. However, the activity of the enzyme once stimulated was decreased gradually by subsequent incubation with the phospholipid at 37°C, reaching a level below the original activity after 1 h of incubation. The presence of ferrous ion almost perfectly protected the enzyme against this phospholipid inactivation. The activity of the enzyme inactivated by incubation with the phospholipid was not only restored, but also increased further by incubation at 37°C with ferrous ion and dithiothreitol. Gel filtration analysis revealed that the enzyme stimulated by phosphatidylinositol was eluted in a void volume together with the phospholipid vesicles, but the enzyme inactivated by incubation with phosphatidylinositol was eluted at a later region apart from the vesicles. These results, taken together, suggest the possible involvement of cellular membranes in the regulation of tryptophan hydroxylase in the central nervous system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07427.x
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  • 55
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    Potassium-Stimulated Release of [3HJTaurine from Cultured GABAergic and Glutamatergic Neurons (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of depolarizing concentrations of potassium (56 mM) on the release of [3H]taurine was examined in two types of cultured neurons from mouse brain: cerebral cortex neurons, which are largely GABAergic, and cerebellar neurons, which after treatment with kainate consist almost entirely of glutamatergic granule cells. The release of [3H]taurine was compared to that of γ-[3H]aminobutyric acid ([3H]GABA) in cortical neurons and to that of D-[3HJaspartate in granule cells. Cortical neurons responded to potassium stimulation (1 min or continuously) by an immediate increase in [3H]GABA efflux of more than six times over the basal efflux, followed by a sharp decline despite the persistence of the stimulatory agent. The potassium-induced release of [3H]GABA was largely calcium-dependent. The release of [3H]taurine was considerably less in magnitude, only doubling after the stimulus, with a time course delayed in both onset and decline. The release of [3H]taurine was partially calcium-dependent and was also decreased in low-chloride solutions. In cerebellar granule cells, exposure to potassium resulted in a large (sixfold) and prompt release of D-[3H]aspartate, largely calcium-dependent. A totally different pattern was observed for the release of [3H]taurine. A stimulatory effect occurred only when cells were exposed continuously to potassium. Taurine efflux was very delayed, with a broad stimulus plateau reached after 15-20 min of stimulation. Taurine release was unaffected by omission of calcium, but it was abolished in a low-chloride medium. These results suggest that taurine is released from cells handling other neuroactive amino acids as neurotransmitters. A co-release of GABA/taurine or glu-tamate/taurine is unlikely due to the marked differences observed’ in their efflux patterns, clearly indicating different mechanisms for release. Instead, taurine release may result from a cell response different from the stimulus-secretion coupling of neurotransmitters.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07429.x
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  • 56
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    Characteristics of Sorbitol Uptake in Rat Glial Primary Cultures (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Uptake of [U-14C]sorbitol was studied in astroglia-rich rat primary cultures. Initial rate of sorbitol uptake is proportional to sorbitol concentration between 20 μM and 400 mM. Sorbitol transport is not inhibited by glucose, fructose, and a variety of structurally related polyols, or by cy-tochalasin B, an inhibitor of glucose transport. Phloretin, phlorizin, filipin, and n-hexanol, all compound that alter the properties of biological membranes, and the sulfhydryl reagent p-chloromercuribenzoate inhibit sorbitol uptake to various degrees. Variation in the concentrations of extracellular Na+ and K+ does not affect transfer of sorbitol across the cell membrane. It is concluded that sorbitol is taken up into glial cells by a diffusion process, not involving a carrier and probably not through the lipid bilayer, but through a proteinaceous channel-like structure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11755.x
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  • 57
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    A Selective Increase in Particulate Superoxide Dismutase Activity in Parkinsonian Substantia Nigra (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The total activity of superoxide dismutase (SOD) and cytosolic and particulate activity of SOD in human substantia nigra and cerebellum were measured by a spectrophotometric method based on the ability of SOD to inhibit the autoxidation of adrenaline. The cystosolic and particulate isoenzymes of SOD were differentiated by the inclusion of potassium cyanide which selectively inhibits cytosolic copper/zinc-dependent SOD activity. In autopsied human brains, there was no difference in total SOD) activity, or the activity of SOD in cytosol in substantia nigra jof patients dying with Parkinson's disease compared to age-matched controls. However, the activity of the particulate form of SOD was higher in the parkinsonian substantia nigra compared to control tissue. In the cerebellum there was no difference in the total, cytosolic, or particulate activity of SOD between parkinsonian patients and age-matched controls. Increased activity of SOD in particulate fraction may be a protective response to elevated levels of toxic free radicals in the parkinsonian substantia nigra. Alternatively, increased SOD activity may induce cell death through the accumulation of hydrogen peroxide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11759.x
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    Isolated Light Chain of Tetanus Toxin Inhibits Exocytosis: Studies in Digitonin-Permeabilized Cells (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Previous work indicates that the heavy chain of tetanus toxin is responsible for the binding of the toxin to the neuronal membrane and its subsequent internalization. In the present study, the light chain of tetanus toxin mimicked the holotoxin in inhibiting Ca2+-dependent secretion of [3H]norepinephrine from digitonin-permeabilized adrenal chromaffin cells. Preincubation of tetanus toxin with monoclonal antibodies to the light chain prevented the inhibition by tetanus toxin. Preincubation of tetanus toxin with nonimmune ascites fluid or with monoclonal antibodies directed against the C fragment (the C-terminal of the heavy chains or the heavy-chain portion of the B fragment did not prevent inhibition by tetanus toxin. The data indicate that the light chain is responsible for the intracellular blockade of exostosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11800.x
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  • 59
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    Effects of Dihydropyridine Calcium Channel Ligands on Rat Brain γ-Aminobutyric AcidB Receptors (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: This study shows that low nanomolar concentrations of the calcium channel antagonist nifedipine displaced [3H]baclofen labeling of γ-aminobutyric acidB (GABAB) receptors, whereas similar concentrations of two calcium channel agonists stimulated this GA-BAB receptor labeling. Neither effect was likely to be due to dihydropyridine (DHP) binding to baclofen recognition sites, because the inhibitory ligand nifedipine primarily affected apparent receptor density rather than affinity. Although these results could reflect the coupling of GABAB receptors with calcium channels, they do not rule out other, possibly more direct interactions between GABAB receptors and DHP binding sites. These DHP effects occur at much lower concentrations and display other significant differences from previously reported effects of DHPs on other transmitter receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11804.x
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  • 60
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    Book Review (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
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    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Book review in this ArticleBrain 5-HT1A Receptors edited by C. J. Dourish, S. Ahlenius, and P. H. Hutson.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11807.x
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  • 61
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    Photoaffinity Labeling and Electrophoretic Identification of the H1-Receptor: Comparison of Several Brain Regions and Animal Species (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The photoaffinity probe [l25I]iodoazidophen-pyramine was used to label irreversibly the H1-receptor in membranes of several guinea pig brain regions and of the cerebral cortex of the rat, mouse, and pig. Following sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis, two main bands were specifically labeled in all tissues: a 56-kilodalton (kDa) peptide and a 41-47-kDa peptide whose relative importance diminished in the presence of protease inhibitors. This indicates that, in all tissues examined, in spite of evidence for pharmacological heterogeneity, the ligand recognition domain of the H1-receptor resides in a 56-kDa peptide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07339.x
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  • 62
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    tele-Methylhistamine Levels and Histamine Turnover in Nuclei of the Rat Hypothalamus and Amygdala (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: An HPLC method using fluorescence detection for the determination of tele-methylhistamine! (t-MH) was improved to a sensitivity level which enabled the detection of 0.05 pmol of tissue t-MH. The t-MH contents and the histamine turnover rates in various nuclei of the rat hypothalamus and amygdala were subsequently measured. The histamine turnover rates were estimated from pargyline-induced t-MH accumulation. Both the t-MH levels and the histamine turnover rates were shown to be relatively high in the nuclei dorsomedialis and premammillaris ventralis of the hypothalamus, and also in the nucleus medialis of the amygdala. The steady-state t-MH levels in various nuclei of the hypothalamus and amygdala correlated well with the histamine turnover rates in these nuclei.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11781.x
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  • 63
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    Light-Induced Dopamine Release from Teleost Retinas Acts as a Light-Adaptive Signal to the Retinal Pigment Epithelium (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In the retinal pigment epithelium (RPE) of lower vertebrates, melanin pigment granules migrate in and out of the cells' long apical projections in response to changes in light condition. When the RPE is in its normal association with the retina, light onset induces pigment granules to disperse into the apical projections; dark onset induces pigment granules to aggregate into the cell bodies. However, when the RPE is separated from the retina, pigment granule movement in the isolated RPE is insensitive to light onset. It thus seems likely that a signal from the retina communicates light onset to the RPE to initiate pigment dispersion. We have examined the nature of this retina-to-RPE signal in green sunfish, Le-pomis cyanellus. In isolated retinas with adherent RPE, light-induced pigment dispersion in the RPE is blocked by treatments known to block Ca2+-dependent transmitter release in the retina. In addition, the medium obtained from incubating previously dark-adapted retinas in the light induces light-adaptive pigment dispersion when added to isolated RPE. In contrast, the medium obtained from incubating dark-adapted retinas in constant darkness does not affect pigment distribution when added to isolated RPE. These results are consistent with the idea that RPE pigment dispersion is triggered by a substance that diffuses from the retina at light onset. The capacity of the conditioned medium from light-incubated retinas to induce pigment dispersion in isolated RPE is in hibited by a D2 dopamine antagonist, but not by D! or α-adrenergic antagonists. Light-induced pigment dispersion in whole RPE-retinas is also blocked by a D2 dopamine antagonist. These results suggest that the diffusible substance is dopamine and that retinal dopamine stimulates pigment dispersion by interacting with D2 dopaminergic receptors on the RPE cell surface. Direct measurement of the endogenous catecholamine content of isolated dark-adapted retinas and of the medium surrounding isolated retinas incubated in the dark or in the light demonstrates that dopamine is the predominant catecholamine of green sunfish retinas, and that light onset stimulates the overflow of endogenous dopamine—but not that of norepinephrine or epinephrine—from isolated retinas. These results suggest that illumination increases dopamine release in teleost retinas. Together, our findings are consistent with the idea that dopamine acts as a paracrinic messenger of light-adaptive stimuli by diffusing from its site of release in the retina to distant nonsynaptic receptors on RPE cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11785.x
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    Peptidasic Activities Associated with Acetylcholinesterase Are Due to Contaminating Enzymes (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The esterasic and peptidasic activities of two different sources of acetylcholinesterase purified from electric eel were examined. Hydrolyses of leucine-enkephalin and neurotensin indicated that both sources exhibited exopepti-dasic and tryptic-like activities. However, the enzyme preparation which appeared 10-fold enriched with regard to the esterasic activity was found to display a 50- and 185-fold lower tryptic-like and exopeptidasic function, respectively. This lack of parallelism in the enrichment of the various activities seemed to indicate that they were not co-purified. Immunoprecipitation experiments performed with monoclonal antibodies directed towards the catalytic subunit of globular or asymmetric forms of electric eel acetylcholinesterase allowed the physical dissociation of esterasic and peptidasic functions and therefore confirmed that the ability of acetylcholinesterase to hydrolyze various neuropeptides was likely due to contaminating peptidases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11793.x
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    Monoclonal Antibody to Embryonic CNS Antigen A2B5 Provides Evidence for the Involvement of Membrane Components at Sites of Alzheimer Degeneration and Detects Sulfatides as Well as Gangliosides (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Immunohistological and biochemical studies were initiated to determine whether or not neural membrane components were associated with degenerative changes characteristic of Alzheimer's disease (AD). Monoclonal antibody A2B5, developed against embryonic chick retinal cells and previously shown to react with neural surface gangliosides, was applied to formalin-fixed sections of control and AD brain tissue. Frontal cortex and hippocampus of AD cases exhibited high levels of A2B5 immunoreactivity within those neurons undergoing neurofibrillary degeneration. Neuritic processes associated with senile plaques were also highly reactive with the A2B5 antibody. The amount of gangliosides and their pattern after HPTLC were the same in control and AD cases. However, the unexpected observation was made that the A2B5 antibody reacted with human brain sulfatides in addition to the expected reactivity with minor gangliosides. The average level of sulfatides in AD brain was significantly higher than in normal controls. The data support the involvement of one or more membrane components with neu-rodegeneration in the Alzheimer brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11798.x
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    Reduced Protein Kinase C Activity in Ischemic Spinal Cord (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Protein phosphorylation was evaluated in a rabbit spinal cord ischemia model under conditions where cyclic AMP-dependent protein kinase (PK-A) and calcium/phos-pholipid-dependent protein kinase (PK-C) were activated. One hour of ischemia did not affect PK-A activity significantly; however, PK-C activity was reduced by more than 60%. In vitro phosphorylation of endogenous proteins by endogenous PK-C revealed that eight particulate and five cytosolic proteins showed stimulated phosphorylation by PK-C activators in control tissue, although this stimulation was virtually absent in ischemic samples. When control and ischemic particulate fractions were combined, the endogenous protein phosphorylation pattern under PK-C-activating conditions was similar to the ischemic sample, which suggests that inhibitory molecules may be present in the ischemic particulate fraction. In vitro phosphorylation of endogenous proteins under PK-A-activating conditions in ischemic tissue was similar to that in control tissue. The results suggest that the PK-C phosphorylation system is selectively impaired in ischemic spinal cord. In addition to reduced PK-C-dependent phosphorylation, an Mr 64,000 protein was phosphorylated in ischemic cytosolic samples, but not in control samples. The phosphorylation of the Mr 64,000 protein was neither PK-C-dependent nor PK-A-dependent. These altered phosphorylation reactions may play critical roles in neuronal death during the course of ischemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb11797.x
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    Changes in Intracellular Free Magnesium During Hypoglycaemia and Hypoxia in Cerebral Tissue as Calculated from 31p-Nuclear Magnetic Resonance Spectra (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: 3lP-nuclear magnetic resonance spectra of super-fused cerebral tissues were obtained under normal, hypogly-caemic, and hypoxic conditions. Concentrations of free intracellular magnesium were calculated from differences in chemical shifts between the α- and β-resonances of the nucleoside phosphates. Control levels of 0.33 mM were significantly increased to 0.52 mM in hypoglycaemia and to 0.57 mM in severe hypoxia. Removal of calcium from the superfusing medium increased the free intracellular Mg2+ concentration to 0.63 mM
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07338.x
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    Identification and Characterization of Calcium-Dependent Metalloproteases in Rat Brain (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We have begun to identify and characterize brain protease activities separated by and assayed in substrate-con-taining polyacrylamide gels. In the present report, we focus on four proteolytic activities identified from rat brain that are dependent on micromolar and millimolar Ca2+ concentrations for activity. In contrast to the previously described Ca2+-dependent neutral cysteine proteases (calpains), all four activities appear to be metalloproteases based on their inhibition by EDTA, EGTA, and 1,10-o-phenanthroline, but not by blockers of serine, cysteine, or aspartic proteases. In the presence of excess Ca2+ and the Zn2+-chelating inhibitor 1,10-o-phenanthroline, activity of the enzymes was reconstituted by addition of lower concentrations of Zn2+, and inhibited by higher Zn2+ concentrations. The four metalloproteases were designated MP-112, MP-92, MP-70, and MP-65 on the basis of their apparent molecular masses in kilodaltons. MP-70, the major activity detected, had an apparent Kact for Ca2+ 〉 100 μM versus 10-25 μM for MP-65 and 50-100 μM for MP-92. MP-112 was a minor activity for which Ca2+ activation levels were not determined. MP-112, MP-70, and MP-65 were similar in being most active in the soluble fraction of 7-day neonate forebrain. In contrast, MP-92 activity was highest in the particulate fraction of adult forebrain. About half of the MP-92 activity and lower levels of the other three activities were still detectable in particulate fractions after detergent extraction of membrane, suggesting an association with cytoskeletal or other structural proteins. These results indicate the presence in CNS of a class of Ca2+-dependent proteases that are distinct from the previously described cal-pains, and that may be important in Ca2+-mediated neural events.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07381.x
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    Comparison of [125I]Iodolysergic Acid Diethylamide Binding in Human Frontal Cortex and Platelet Tissue (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The human platelet contains a functional 5-hy-droxytryptamine (5-HT) receptor that appears to resemble the 5-HT2 subtype. In this study, we have used the iodinated derivative [I25I]iodolysergic acid diethylamide ([I25I]iodoLSD) in an attempt to label 5-HT receptors in human platelet and frontal cortex membranes under identical assay conditions to compare the sites labelled in these two tissues. In human frontal cortex, [125I]iodoLSD labelled a single high-affinity site (KD= 0.35 ± 0.02 nM). Displacement of specific [l25I]iodoLSD binding indicated a typical 5-HT2 receptor inhibition profile, which demonstrated a significant linear correlation (r= 0.97, p 〉 0.001, n = 17) with that observed using [3H]ketanserin. However, [125I]iodoLSD (Bmax= 136 ± 7 fmol/mg of protein) labelled significantly fewer sites than [3H]ketanserin (Bmax= 258 ± 19 fmol/mg of protein) (p 〉 0.001, n = 6). In human platelet membranes, [125I]iodoLSD labelled a single site with affinity (KD= 0.37 ± 0.03 nM) similar to that in frontal cortex. The inhibition profile in the platelet showed significant correlation with that in frontal cortex (r.= 0.96, p 〉 0.001, n = 16). We conclude that the site labelled by [125I]iodoLSD in human platelet membranes is biochemically similar to that in frontal cortex and most closely resembles the 5-HT2 receptor subtype, although the discrepancy in binding capacities of [125I]iodoLSD and [3H]ketanserin raises a question about the absolute nature of this receptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07313.x
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    Changes in Cholinergic but Not in GABAergic Markers in Amygdala, Piriform Cortex, and Nucleus Basalis of the Rat Brain Following Systemic Administration of Kainic Acid (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Three days after systemic administration of kainic acid (15 mg/kg, s.c), selected cholinergic markers (choline acetyltransferase, acetylcholinesterase, muscarinic acetylcholine receptor, and high-affinity choline uptake) and GABAergic parameters [benzodiazepine and γ-aminobutyric acid (GABA) receptors] were studied in the frontal and piriform cortex, dorsal hippocampus, amygdaloid complex, and nucleus basalis. Kainic acid treatment resulted in a significant reduction of choline acetyltransferase activity in the piriform cortex (by 20%), amygdala (by 19%), and nucleus basalis (by 31%) in comparison with vehicle-injected control rats. A lower activity of acetylcholinesterase was also determined in the piriform cortex following parenteral kainic acid administration. [3H]Quinuclidinyl benzilate binding to muscarinic acetylcholine receptors was significantly decreased in the piriform cortex (by 33%), amygdala (by 39%), and nucleus basalis (by 33%) in the group treated with kainic acid, whereas such binding in the hippocampus and frontal cortex was not affected by kainic acid. Sodium-dependent high-affinity choline uptake into cholinergic nerve terminals was decreased in the piriform cortex (by 25%) and amygdala (by 24%) after kainic acid treatment. In contrast, [3H]flunitrazepam binding to benzodiazepine receptors and [3H]muscimol binding to GABA receptors were not affected 3 days after parenteral kainic acid application in any of the brain regions studied. The data indicate that kainic acid-induced limbic seizures result in a loss of cholinergic cells in the nucleus basalis that is paralleled by degeneration of cholinergic fibers and choli-noceptive structures in the piriform cortex and amygdala, a finding emphasizing the important role of cholinergic mechanisms in generating and/or maintaining seizure activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07316.x
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    In Vivo Measurement of Extracellular 5-Hydroxytryptamine in Hippocampus of the Anaesthetized Rat Using Microdialysis: Changes in Relation to 5-Hydroxytryptaminergic Neuronal Activity (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of manipulating the activity of central 5-hydroxytryptamine (5-HT) neurones on extracellular 5-HT in ventral hippocampus of the chloral hydrate-anaesthetized rat was studied using the brain perfusion method, microdialysis. Basal levels of 5-HT in the dialysates were close to the detection limits of our assay using HPLC with electrochemical detection. However, addition of the selective 5-HT reuptake inhibitor citalopram (10−6M) to the perfusion medium produced readily measurable amounts of dialysate 5-HT. Citalopram, therefore, was used throughout our experiments. Hippocampal dialysate levels of 5-HT sharply declined over the first hour after dialysis probe implantation, but then became constant. This stable output of 5-HT was reduced by 57% in rats treated 14 days previously with intracerebroven-tricular injections of the 5-HT neurotoxin 5,7-dihydroxy-tryptamine. Electrical stimulation (1-ms pulse width, 300 μA, 2–20 Hz) of the dorsal raphe nucleus for 20 min caused a rapid rise in hippocampal 5-HT output, which immediately declined on cessation of the stimulus and was frequency-dependent. Addition of tetrodotoxin (10−6M) to the perfusion medium reduced 5-HT levels to 75% of predrug values. Injection of the 5-HT1A agonist 8-hydroxy-2-(di-n-propylami-no)tetralin (0.5 and 2.5 μg) into the dorsal raphe nucleus caused a dose-related fall in hippocampal output of 5-HT compared to saline-injected controls. We conclude from these data that the spontaneous output of endogenous 5-HT into hippocampal dialysates, measured under our experimental conditions, predominantly originates from central 5-HT neurones and changes in accordance with their electrical activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07319.x
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    Comparison of Excitatory Amino Acid-Stimulated Phosphoinositide Hydrolysis and N-[3H]Acetylaspartylglutamate Binding in Rat Brain: Selective Inhibition of Phosphoinositide Hydrolysis by 2-Amino-3-Phosphonopropionate (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The activation of phosphoinositide hydrolysis by ibotenate (IBO) in brain slices and the binding of N-[3H]acetylaspartyl-L-glutamate (NAAG) to brain membranes are biochemical parameters previously shown to be selectively inhibited by 2-amino-4-phosphonobutyrate (AP4). We have examined whether the binding of [3H]NAAG and stimulation of phosphoinositide hydrolysis by IBO are indexing the same or different populations of AP4-sensitive excitatory amino acid sites in brain. L-AP4 and D,L-2-amino-3-phosphono-propionate (D,L-AP3) were found to be about equipotent inhibitors of IBO-stimulated phosphoinositide hydrolysis. L-AP4 and D,L-AP3 did not inhibit stimulation of phosphoinositide hydrolysis by the cholinoceptor agonist carbachol. The L-isomers of serine-O-phosphate and α-aminoadipate were selective inhibitors of IBO-stimulated phosphoinositide hydrolysis, but were less potent than L-AP4 or D,L-AP3. When these compounds were examined for their ability to inhibit [3H]NAAG binding to membranes of rat forebrain, the relative order of potency was L-α-aminoadipate = D-α-aminoadipate 〈 L-AP4 〈 L-serine-O-phosphate 〈 D-AP4 〈 D,L-AP3. Concentrations of NAAG up to 10−2M did not stimulate phosphoinositide hydrolysis. Thus, although both assays are sensitive to L-AP4 inhibition, they appear to represent disparate excitatory amino acid sites in brain. Furthermore, D,L-AP3 appears to be a more selective inhibitor of excitatory amino acid-stimulated phosphoinositide hydrolysis than L-AP4, and might be a more useful pharmacological tool to define the function of these receptor sites in brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07324.x
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    Direct Evidence That Excitotoxicity in Cultured Neurons Is Mediated via N-Methyl-D-Aspartate (NMDA) as well as Non-NMDA Receptors (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Cultured GABAergic cerebral cortex neurons were exposed to the excitatory amino acid (EAA) L-glutamate, kainate (KA), N-methyl-D-aspartate (NMDA), or RS-α-amino-3-hydroxy-5-methyl-4-isoxazolopropionate (AMPA). To ensure a constant glutamate concentration in the culture media during the exposure periods, the glutamate uptake inhibitor L-aspartic acid β-hydroxamate was added at 500 μM to the cultures that were exposed to glutamate. Each of these EAAs was able to induce neurotoxicity. It was not possible to reduce or prevent glutamate-induced cytotoxicity by blocking only one of the glutamate receptor subtpes with either the NMDA receptor antagonist D-(-)-2-amino-5-phosphonopentanoate (APV) or with one of the specific non-NMDA antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 6,7-dinitroquinoxaline-2,3-dione (DNQX). However, if the cultures were exposed simultaneously to glutamate and the antagonists in combination, i.e., APV plus CNQX or APV plus DNQX, the toxicity was completely prevented. Furthermore, CNQX and DNQX were shown to be selective blockers of cytotoxic phenomena induced by non-NMDA glutamate agonists with no effect on NMDA-induced cell death. Likewise, APV prevented NMDA-induced cell death without affecting the KA- or AMPA-induced neurotoxicity. It is concluded that EAA-dependent neurotoxicity is induced by NMDA as well as non-NMDA receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07327.x
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    In Vivo Measurement Using Microdialysis of the Release and Metabolism of 5-Hydroxytryptamine in Raphe Neurones Grafted to the Rat Hippocampus (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The overflow and metabolism of serotonin (5-hydroxy-tryptamine; 5-HT) from transplants of embryonic medullary and mesencephalic raphe neurones in the previously 5-HT-denervated hippocampus have been analyzed in vivo using intracerebral dialysis. The average density of 5-HT-immunoreactive fibres in the grafted hippocampus was less than in nonlesioned hippocampus. Nonetheless, both basal and potassium-stimulated levels of 5-HT in the dialysates were restored to approximately normal after transplantation of medullary raphe cells, whereas mesencephalic implants resulted in over twice the 5-HT output observed in control hippocampus. However, 5-hydroxyindoleacetic acid (5-HIAA) overflow was increased only after grafting of mesencephalic raphe and then only to normal levels; medullary implants, by contrast, failed to enhance 5-HIAA output above that from lesion-only hippocampus. The evidence of a relative hyperactivity of the grafted neurones may explain the disproportionate improvements in various lesion-induced behavioural deficits after grafting of nervous tissue. In addition, differences in the presynaptic regulation of 5-HT release and metabolism are also apparent in the transplants; these variations are dependent on the precise origin of the serotoninergic cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07329.x
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    Serotonin 5-HT2 Receptors: Two States Versus Two Subtypes (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), 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.1471-4159.1989.tb07334.x
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    Classification of Abstracts by Session (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), 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.1471-4159.1989.tb13275.x
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    Muscarinic Receptor Stimulation Increases Inositol-Phospholipid Metabolism and Inhibits Cyclic AMP Accumulation in PC 12 Cells (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Muscarinic receptor stimulation increased the accumulation of 3H-inositol phosphates in PC12 cells whose phospholipids had been prelabeled with [3H]inositol. Muscarine also inhibited the increase in cyclic AMP (cAMP) accumulation caused by 5′-N-ethylcarboxamide adenosine or by vasoactive intestinal peptide. This effect of muscarine was apparently due to the inhibition of adenylate cyclase rather than to a stimulation of a cAMP specific phosphodiesterase. The muscarinic receptor antagonist pirenzepine inhibited both the stimulation of inositol-phospholipid metabolism and the inhibition of cAMP production with Ki values of 0.34 μM and 0.36 μM, respectively. PC 12 cells contained a single class of N-[3H]methylscopolamine ([3H]NMS) binding sites. Competition studies with muscarine (KD, 15 μM) and pirenzepine (Ki; 0.12 μM) revealed no evidence for multiple muscarinic receptors. The Ki of pirenzepine for the inhibition of [3H]NMS binding and the inhibition of muscarinic actions is consistent with the possibility that this is not an Mi receptor. Muscarine inhibited cAMP accumulation in cells made de ficient in protein kinase C; therefore, this protein kinase is probably not involved in mediating the inhibitory effect of muscarine. The phorbol ester 12-O-tetradecanoylphorbol 13-acetate also inhibited cAMP accumulation in PC12 cells but the mechanism of this effect differed from that of muscarine. Bradykinin caused a large increase in the accumulation of3H-inositol phosphates and [3H]diacylglycerol relative to muscarine but did not inhibit cAMP production. Oxotrem-orine inhibited cAMP accumulation but it did not stimulate inositol-phospholipid metabolism. These data indicate that increased inositol-phospholipid metabolism and inhibition of cAMP production are two independent effects of muscarinic receptor stimulation in PC12 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07314.x
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    Muscarinic Agonists Cause Calcium Influx and Calcium Mobilization in Forebrain Neurons In Vitro (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We have examined the effects of the muscarinic agonist carbachol on the intracellular free Ca2+ concentration ([Ca2+]i) in primary cultures of neurons from rat forebrain using the Ca2+-sensitive fluorescent dye fura-2. Addition of carbachol increased the [Ca2+]i in ∼60% of cells studied. Oxotremorine-M, but not pilocarpine, mimicked the effects of carbachol. The response was reduced by 60% on removal of extracellular Ca2+, a finding suggesting that muscarinic receptor activation causes Ca2+ influx in addition to intracellular Ca2+ mobilization. Tetrodotoxin and nitrendipine also significantly reduced the response to carbachol. These studies suggest that the changes in [Ca2+]i produced by activation of muscarinic receptors result in part from mobilization of intracellular Ca2+ and that influx through voltage-sensitive Ca2+ channels also provides a significant contribution to the net [Ca2+]i change observed
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07318.x
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    Modification of Gs-Stimulated Adenylate Cyclase in Brain Membranes by Low pH Pretreatment: Correlation with Altered Guanine Nucleotide Exchange (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Pretreatment of rat brain membranes at pH 4.5 before assay at pH 7.4 modifies the function of GTP-binding proteins (G-proteins) by eliminating Gs-stimulated adenylate cyclase activity while increasing opiate-inhibited adenylate cyclase activity. To help characterize the molecular nature of the low pH effect, we labeled Gs and Gi a-subunits in both control and low pH-pretreated membranes with the GTP photoaffinity analog [32P]P3(4-azidoanilido)-P1-5′-GTP ([32P]AAGTP). When membranes were preincubated with unlabeled AAGTP, a persistent inhibitory state of adenylate cyclase was produced, which was overcome in untreated membranes with high (〈 1 μM) concentrations of guanylyl-5′-imidodiphosphate [Gpp(NH)p]. In low pH-pretreated membranes, this inhibition could not be overcome, and stimulation by Gpp(NH)p was eliminated. Maximal inhibition of adenylate cyclase achieved by incubation with AAGTP was not altered by low pH pretreatment. Incorporation of [32P]AAGTP into Gs (42 kilodaltons) or Gi/G (40 kilodaltons) was unaffected by low pH pretreatment; however, transfer of 32P from Gi/o to Gs, which occurs with low (10 nM) concentrations of Gpp(NH)p in untreated membranes, was severely retarded in low pH-pretreated membranes. Both the potency and efficacy of Gpp(NH)p in producing exchange of [32P]AAGTP from Gi/0 to Gs were markedly reduced by low pH pretreatment. These results correlate the loss of Gs-stimulated adenylate cyclase with a loss of transfer of nucleotide from Gi/0 to Gsα-subunits and suggest that the nucleotide exchange participates in the modulation of neuronal adenylate cyclase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07317.x
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  • 80
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    Aluminum Increases Agonist-Stimulated Cyclic AMP Production in Rat Cerebral Cortical Slices (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effects of A1C13 on basal and stimulated cyclic AMP production in rat cerebral cortical slices were studied. AICI3 (10–250 μM) had no effect on the cyclic AMP concentration in the absence of drugs that stimulate the synthesis of cyclic AMP. 2-Chloroadenosine (25–200 μM) significantly stimulated the synthesis of cyclic AMP in a concentration-dependent manner, and A1C13 significantly potentiated this response at 50 and 100 μM 2-chloroadenosine. This effect of AICI3 was dependent on preexposure of the slices to A1C13 before addition of the agonist. The potentiation by A1C13 of the 2-chloroadenosine-induced increase in cyclic AMP level was concentration dependent, with significant enhancement by 100 (142% of the control) and 250 (150% of the control) μM AICI3. Lower concentrations of A1C13 had no significant effect on the production of cyclic AMP stimulated by 2-chloroadenosine. AICI3 also potentiated the isoproterenol-induced increase in cyclic AMP production. Forskolin-induced production of cyclic AMP was unaltered by the presence of A1C13. These results demonstrate that A1C13 can potentiate agonist-stimulated cyclic AMP production in a whole-cell brain preparation without the addition of fluoride. This may account for the previously reported aluminum-induced increase in cyclic AMP concentrations in rat brain in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07322.x
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  • 81
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    Regulation of Substance P Receptor Affinity by Guanine Nucleotide-Binding Proteins (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The binding of substance P (SP) to receptors in peripheral tissues as well as in the CNS is subject to regulation by guanine nucleotides. In this report, we provide direct evidence that this effect is mediated by a guanine nucleotide-binding regulatory protein (G-protein) that is required for high-affinity binding of SP to its receptor. Rat submaxillary gland membranes bind a conjugate of SP and I25I-labeled Bolton-Hunter reagent (125I-BHSP) with high affinity (KD= 1.2 ± 0.4 × 10−9M) and sensitivity to guanine nucleotide inhibition. Treatment of the membranes with alkaline buffer (pH 11.5) causes a loss of the high-affinity, GTP-sensitive binding of l25I-BHSP and a parallel loss of [35S]guanosine 5′-(3-O-thio)triphosphate ([35S]GTPγS) binding activity. Addition of purified G-proteins from bovine brain to the alkaline-treated membranes restores high-affinity 125I-BHSP binding. Reconstitution is maximal when the G-proteins are incorporated into the alkaline-treated membranes at a 30-fold stoichiometric excess of GTPγS binding sites over SP binding sites. Both Go (a pertussis toxin-sensitive G-protein having a 39,000-dalton α-subunit) and Gi (the G-protein that mediates inhibition of adenylate cyclase) appear to be equally effective, whereas the isolated α-subunit of Go is without effect. The effects of added G-proteins are specifically reversed by guanine nucleotides over the same range of nucleotide concentrations that decreases high-affinity binding of 125I-BHSP to native membranes. Although our results indicate that SP receptors in rat submaxillary gland membranes are coupled to a G-protein that possesses a nucleotide specificity similar to that of Go/Gi, the relevant G-protein appears to differ from Go and Gi in terms of its sensitivity to pertussis toxin treatment. Reconstitution methods described should be useful in future studies to purify this G-protein and to analyze further its interaction with the SP receptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07323.x
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  • 82
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    Abstracts in Session Order (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), 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.1471-4159.1989.tb13274.x
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  • 83
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    Stimulation of D-2 Dopamine Receptors Decreases the Evoked In Vitro Release of [3H] Acetylcholine from Rat Neostriatum: Role of K+ and Ca2+ (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Reportedly, stimulation of D-2 dopamine receptors inhibits the depolarization-induced release of acetylcholine from the neostriatum in a cyclic AMP-independent manner. In the present study, we investigated the role of K+ and Ca2+ in the D-2 receptor-mediated inhibition of evoked [3H]acetylcholine release from rat striatal tissue slices. It is shown that the D-2 receptor-mediated decrease of K+-evoked [3H]acetylcholine release is not influenced by the extracellular Ca2+ concentration. However, increasing extracellular K+, in the presence and absence of Ca2+, markedly attenuates the effect of D-2 stimulation on the K+-evoked [3H]acetylcholine release. Furthermore, it is shown that activation of D-2 receptors in the absence of Ca2+ also inhibits the veratrine-evoked release of [3H]acetylcholine from rat striatum. These results suggest that the D-2 dopamine receptor mediates the decrease of depolarization-induced [3H]acetylcholine release from rat striatum primarily by stimulation of K+ efflux (opening of K+ channels) and inhibition of intracellular Ca2+ mobilization.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07244.x
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  • 84
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    Acetylcholine Synthesis by a Sympathetic Ganglion in the Presence of 2-(4-Phenylpiperidino)cyclohexanol (AH5183) and Picrylsulfonic Acid (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The present experiments measured the release and the synthesis of acetylcholine (ACh) by cat sympathetic ganglia in the presence of 2-(4-phenylpiperidino)cyclohexanol (AH5183 or vesamicol) and/or picrylsulfonic acid (TNBS), two compounds known to have the ability to block the uptake of ACh by cholinergic synaptic vesicles in vitro. We confirmed that, in stimulated (5 Hz) perfused (30 min) ganglia, AH5183 depressed ACh release and ACh tissue content increased by 86 ± 6% compared to contralateral ganglia used as controls. Preganglionic activity increased ACh release by a similar amount in the presence (19.9 ± 1.0 pmol/min) or absence (20.5 ± 2.4 pmol/min) of TNBS. The final tissue ACh content was also similar in the presence (1,668 ± 166 pmol) or absence (1,680 ± 56 pmol) of TNBS. However, the AH5183-induced increase of tissue ACh content (86 ± 6%) was abolished completely when AH5183 was perfused with 1.5 mM/TNBS (-3.0 ± 1.0%). This inhibition of ACh synthesis, observed in TNBS-AH5183-perfused ganglia, was not dependent upon further inhibition of ACh release beyond that caused by AH5183 alone, because 14.0 ± 1.9% of the transmitter store was released by preganglionic nerve stimulation in the presence of TNBS plus AH5183 and this was similar in the presence of AH5183 without TNBS (14.0 ± 0.6%). Moreover, when ganglia were first treated with TNBS and then stimulated in the presence of AH5183, an increase of 64 ± 6% of the ganglionic ACh content occurred, and this increase was not statistically different from the increase measured with AH5183 alone (86 ± 6%). Conversely, when ganglia were perfused first with AH5183 and then with TNBS during preganglionic stimulation, no change in the final tissue ACh content was observed, suggesting that AH5183 must be present inside the cells for the inhibitory action of TNBS to be manifest. Moreover, after perfusion of ganglia with [3H]choline, the specific activity of ACh was greater in ganglia treated with AH5183 (76 ± 3 dpm/pmol) than in ganglia treated with TNBS plus AH5183 (48 ± 4 dpm/pmol), whereas the specific activity of choline was less (23 ± 3 and 47 ± 7 dpm/pmol, respectively), suggesting that the enzyme choline acetyltransferase might be inhibited. Considering that TNBS acts extracellularly on the membrane and AH5183 intracellularly on the vesicles, these results suggest that the interaction between the two compounds might well occur during exocytosis and, if the phenomenon involves choline acetyltransferase inhibition, it is presumably a membrane-associated pool of enzyme that is affected.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07245.x
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  • 85
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    High-Affinity Cannabinoid Binding Site: Regulation by Ions, Ascorbic Acid, and Nucleotides (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The high-affinity cannabinoid site in rat brain is an integral component of brain membranes that recognizes cannabinoids with inhibitory constants (Ki) in the nanomolar range. To clarify its physiological role, we studied the regulation of [3H]5′-trimethylammonium Δ8-tetrahydrocannabinol ([3H]TMA) binding. The site is inhibited by heavy metal ions, such as La3+, at low micromolar concentrations; divalent cations, such as Ca2+ and Mg2+, inhibit [3H]TMA binding, though at somewhat higher concentrations. In contrast, [3H]TMA binding is stimulated by Fe2+, Cu2+, and Hg2+ ions. Ascorbic acid and its analogs are also stimulators of cannabinoid binding at low micromolar concentrations. Stimulation of [3H]TMA binding by ascorbate or ions is dependent upon molecular oxygen, but is not inhibited by metabolic poisons. Metabolically stable nucleoside triphosphate analogs enhance [3H]TMA binding by different mechanisms, with hydrolysis of a high-energy phosphate bond apparently requisite for these influences. These results suggest that the cannabinoid binding site is associated with a nucleotide-utilizing protein possessing multiple regulatory subsites.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07273.x
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  • 86
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    Tachykinin Receptors of the NK1 Type (Substance P) Coupled Positively to Phospholipase C on Cortical Astrocytes from the Newborn Mouse in Primary Culture (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Specific 125I-Bolton-Hunter substance P (125I-BHSP) binding sites are present on intact cortical astrocytes of the newborn mouse in primary culture. Therefore, these cells were used to ascertain the existence of functional substance P (SP) receptors coupled positively to phospholipase C. SP stimulated phosphoinositide breakdown with an EC50 value (4.5 × 10−10M) similar to its IC50 value (3.8 × 10−10M) for inhibiting 125I-BHSP binding. The maximal response (to 10−6M SP for 60 min) obtained was ∼500% of control values. The rank order of potency of tachykinins was SP 〉 neurokinin (NK) A 〉 NKB. Long SP C-terminal fragments were more potent than shorter ones in stimulating the accumulation of 3H-inositol phosphates. SP free acid and SP N-terminal fragments were without effect. [L-Pro9]SP and SP methyl ester, two selective agonists of NK1 receptors, were almost as potent as SP. An excellent correlation was found when the abilities of tachykinins and their analogs for stimulating phosphoinositide breakdown and for inhibiting 125I-BHSP binding were compared. Finally, when used at a concentration of 3 × 10−6M, spantide ([D-Arg1, D-Trp7,9, Leu11]SP), an SP antagonist, competitively reduced the stimulatory effect of SP on accumulation of 3H-inositol phosphates. These results demonstrate the presence of functional SP receptors (NK1) on cortical astrocytes from the newborn mouse in primary culture.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07276.x
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  • 87
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    N-Methyl-D-Aspartate Receptors and Ethanol: Inhibition of Calcium Flux and Cyclic GMP Production (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Measurements of calcium uptake and cyclic GMP production by cerebellar granule cells grown in primary culture demonstrated that ethanol preferentially inhibited N-methyl-D-aspartate (NMDA) receptor-gated cation channel function. Concentrations of ethanol as low as 10 mM inhibited NMDA-stimulated Ca2+ uptake by 〉30%, and ethanol also inhibited NMDA-stimulated (Ca2+-dependent) cyclic GMP accumulation in a similar, dose-dependent manner. Responses to kainate were significantly less sensitive to ethanol. Studies using various concentrations of NMDA, as well as phencyclidine (PCP) and glycine, suggested that ethanol affected the “coagonist” binding site of the NMDA receptor-channel complex, rather than the PCP recognition site.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07280.x
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  • 88
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    Determination of Brain Interstitial Concentrations by Microdialysis (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Microdialysis is an extensively used technique for the study of solutes in brain interstitial space. The method is based on collection of substances by diffusion across a dialysis membrane positioned in the brain. The outflow concentration reflects the interstitial concentration of the substance of interest, but the relationship between these two entities is at present unclear. So far, most evaluations have been based solely on calibrations in saline. This procedure is misleading, because the ease by which molecules in saline diffuse into the probe is different from that of tissue. We describe here a mathematical analysis of mass transport into the dialysis probe in tissue based on diffusion equations in complex media. The main finding is that diffusion characteristics of a given substance have to be included in the formula. These include the tortuosity factor (λ) and the extracellular volume fraction (α). We have substantiated this by studies in a welldefined complex medium (red blood cell suspensions) as well as in brain. We conclude that the traditional calculation procedure results in interstitial concentrations that are too low by a factor of λ2/α for a given compound.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07252.x
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  • 89
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    Release of γ-[3H]Aminobutyric Acid from Rat Olfactory Bulb and Substantia Nigra: Differential Modulation by Glutamic Acid (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We have studied the glutamate modulation of γ-[3H]aminobutyric acid ([3H]GABA) release from GABAergic dendrites of the external plexiform layer of the olfactory bulb and from GABAergic axons of the substantia nigra. In the olfactory bulb, [3H]GABA release was induced by high K+ and kainate, and not by aspartate and glutamate alone. However, when the tissue was conditioned by a previous K+ depolarization, glutamate and aspartate caused [3H]GABA release. The effect of glutamate was significantly enhanced when the GABA uptake mechanism was blocked by nipecotic acid. N-Methyl-D-aspartate and quisqualate did not cause [3H]GABA release under the same conditions. The acidic amino acid receptor antagonist 2-amino-4-phosphonobutyric acid and the N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonovaleric acid significantly inhibited the K+-glutamate- and the kainate-induced [3H]GABA release. Mg2+ (5 mM), which blocks the N-methyl-D-aspartate receptors, significantly inhibited the K+-glutamate-induced but not the kainic acid-induced [3H]GABA release. The K+-glutamate-stimulated release, but not the K+-stimulated [3H]GABA release, was strongly inhibited by Na+-free solutions or by 300 nM tetrodotoxin. Apparently the glutamateinduced release of [3H]GABA occurs through an interneuron because it is dependent on the presence of nerve conduction. In the substantia nigra no [3H]GABA release was elicited by any of the glutamate agonists tested. The present results clearly differentiate between the effects of glutamate on the release of [3H]GABA from the substantia nigra and from the olfactory bulb. It is possible that in the external plexiform layer of the olfactory bulb there is a mixed population of voltage-dependent excitatory amino acid receptors, capable of modulating GABA release through an interneuron. In the substantia nigra glutamate does not modulate GABA release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07255.x
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  • 90
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    Frontal Cortical and Left Temporal Glutamatergic Dysfunction in Schizophrenia (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Glutamatergic mechanisms have been investigated in postmortem brain samples from schizophrenics and controls. D-[3H]Aspartate binding to glutamate uptake sites was used as a marker for glutamatergic neurones, and [3H]kainate binding for a subclass of postsynaptic glutamate receptors. There were highly significant increases in the binding of both ligands to membranes from orbital frontal cortex on both the left and right sides of schizophrenic brains. The changes are unlikely to be due to antemortem neuroleptic drug treatment, because no similar changes were recorded in other areas. A predicted left-sided reduction in D-[3H]aspartate binding was refuted at 5% probability, but not at 10%. Previously reported high concentrations of dopamine in left amygdala were strongly associated with low concentrations of D-[3H]aspartate binding in left polar temporal cortex in the schizophrenics. The findings are compatible with an overabundant glutamatergic innervation of orbital frontal cortex in schizophrenia. The results also suggest that schizophrenia may involve left-sided abnormalities in the relationship between temporal glutamatergic and dopaminergic projections to amygdala.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07257.x
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  • 91
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    Is the Augmentation of K+-Evoked Intrasynaptosomal Ca2+ Concentration Due to the Influx of Ca2+ in Rat Brain Synaptosomes? (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Intraterminal free Ca2+ concentration modulates the subsequent release of neurotransmitters. Depolarization of synaptosomes with 29 mM K+ augments cytosolic free Ca2+ concentration, which is triphasic, the peak times being at 10, 60, and 180 s. We examined the characteristics of each elevation of cytosolic free Ca2+ concentration in rat brain synaptosomes which had been preincubated for 3 min with a Ca2+-channel blocker, such as La3+, diltiazem, nifedipine, or verapamil, and under conditions of hypoxia or acidosis. The concentration of free Ca2+ in the quin-2-loaded rat brain synaptosomes was detected fluorometrically. All these elevations were suppressed in the presence of 200 μM EGTA or 100 μM La3+. At the first phase, the elevation of cytosolic free Ca2+ concentration with high K+ stimuli was significantly inhibited by La3+ (20 μM) or by acidosis (pH 6.7). On the other hand, diltiazem, which is a more potent blocker of the release of Ca2+ from the mitochondria, inhibited the increasing cytosolic free Ca2+ concentration at the third phase in a concentration-dependent manner. Hypoxia also showed inhibition at the third phase. These results suggest that the augmentation of high K+-evoked cytosolic free Ca2+ concentration may be due to the influx of extracellular Ca2+. The increase in cytosolic free Ca2+ concentration at the third phase is no doubt linked to the mitochondrial function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07265.x
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  • 92
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    Presynaptic Mechanisms Underlying the γ-Aminobutyric Acid-Evoked Receptor-Independent Release of [3H]Norepinephrine in Rat Hippocampus (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effects of γ-aminobutyric acid (GABA) on the spontaneous efflux of [3H]norepinephrine ([3H]NE) were studied in synaptosomes prepared from rat hippocampus and prelabelled with [3H]NE. It had been observed previously that, when synaptosomes were exposed in superfusion to GABA, the basal release of the tritiated catecholamine was enhanced, apparently with no involvement of the known GABA receptors. The mechanisms underlying this effect have now been investigated. The potency of GABA as a releaser of [3H]NE was decreased by lowering the Na+ content of the superfusion medium, and its effect disappeared at 23 mM Na+. The GABA-induced [3H]NE release was counteracted by the GABA uptake inhibitor N-(4,4-diphenyl-3-butenyl)nipecotic acid (SKF 89976A), but it was unaffected by the NE uptake blockers desmethylimipramine and nisoxetine. The GABA-induced release of [3H]NE was Ca2+-dependent and tetrodotoxin-sensitive. The data support the hypothesis that GABA provoked [3H]NE release by a novel mechanism which involves penetration into the noradrenergic nerve terminals through a GABA carrier located on the NE terminals themselves. This uptake process might be electrogenic and provoke depolarization of the nerve terminals, causing an exocytotic release of [3H]NE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07267.x
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  • 93
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    Formation of Ganglioside GD 1b-Lactone in Rat Brain from Intracisternally Administered GD 1b (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The presence of ganglioside GD1b, in lactone form GD1b-L, was ascertained in rat brain. The possible formation of GD1b-L from GD1b in brain was explored by the intracisternal injection of GD1b, 3H-labelled at the level of the terminal galactose. This was followed by recognition of the radioactive gangliosides formed at different times (1,3, and 7 days) after injection. Whereas at 0 time after injection the only radioactive ganglioside was GD1b, after 1, 3, and 7 days other radioactive gangliosides were also found, thus indicating GD1b penetration into the brain tissue, followed by metabolic processing. Besides GD1b, the following radioactive gangliosides were recognized: GM1 and GM2, derived from GD1b degradation; GT1b, formed by the direct sialylation of GD1b; and GD1b-L, produced by metabolic lactonization. The radioactivity carried by GD1b-L was maximal 3 days after injection; its time course was different from that of the other gangliosides, suggesting that the process of lactonization is separate from that of both degradation and glycosylation. Under the same experimental conditions, some radioactive gangliosides also appeared in the liver, although in much smaller amounts than in brain. Radioactive GD1b-L could not be detected in liver, thus indicating that metabolic lactonization is a tissue- or organ-specific process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09186.x
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  • 94
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    Calcitonin Gene-Related Peptide-Binding Sites of Porcine Cardiac Muscles and Coronary Arteries: Solubilization and Characterization (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Calcitonin gene-related peptide (CGRP)-binding sites were solubilized, using digitonin, from the porcine spinal cord, atria, and coronary arteries. The specific binding of 125I-human α-CGRP to the solubilized binding sites was inhibited by human α- and β-CGRP and by rat α-CGRP, but not by angiotensin II or human calcitonin. Scatchard plot analysis of saturation gave the same KD value for CGRP in the crude membrane fractions of the tissues examined. The affinity of CGRP to the binding sites was decreased by solubilization in the atria and coronary arteries, but not in the spinal cord. Affinity labeling followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed distinct molecular sizes of the specific binding sites among the tissues; 70K for the spinal cord, 70K and 90K for the coronary arteries, and 70K and 120K for the atria. These results indicate that the molecular characteristics of the specific binding sites of CGRP in the cardiovascular system are distinct from those in the central nervous system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07277.x
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  • 95
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    Inactivation of Cyclic AMP-Dependent Taurine Release from Astroglia (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: When astroglial cells are exposed to β-adrenergic agonists for long periods of time (〉20 min), transient increases in taurine release and intracellular cyclic AMP (cAMP) are observed. Three phases of taurine release can be distinguished: activation, inactivation, and an elevated steady state. In this article, we present data describing the relationship between intracellular cAMP levels and inactivation of taurine release. To do this, we compared the apparent first-order rate constants for the inactivation of taurine release (ktau) with the apparent first-order rate constant for the decline of intracellular cAMP (kCAMP). We also measured ktau under experimental conditions that were chosen to provide a wide range of intracellular cAMP concentrations or to stimulate release without the involvement of the β-adrenergic receptor and adenylate cyclase. When taurine release was stimulated with a saturating concentration of isoproterenol, the inactivation of release was significantly faster than the decline of intracellular cAMP. Furthermore, there were no significant differences in ktau measured under any of the experimental conditions used. Thus, inactivation of taurine release does not involve changes in the activity of the β-adrenergic receptor and adenylate cyclase, i.e., desensitization, and appears to be independent of the intracellular concentration of cAMP. These results indicate that cAMP-mediated events can be regulated by mechanism(s) in addition to those that control receptor-adenylate cyclase interactions and the synthesis of cAMP. Such regulation may occur by inactivation of protein kinase A activity or the taurine transport mechanism or by activation of a phosphoprotein phosphatase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09193.x
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  • 96
    Electronic Resource
    Electronic Resource
    Postnatal Development and Possible Ligand Function of the CNS-Specific Membrane Glycoprotein CNSgp 130 (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: CNSgp 130 is a CNS-specific membrane glycoprotein present in large amounts in the adult mammalian CNS. Using immunohistological techniques, we demonstrated that CNSgp 130 is not detectable in the rat cerebellum at birth, and does not appear in the cerebellum until the tenth day of postnatal life. It is expressed first in the white matter of the cerebellar folia, and subsequently (by day 14) it is expressed also in the molecular layer. Expression in the granular layer is not seen until the 18th day of postnatal life, by which time the adult pattern of expression is established. CNSgp 130 is also not detectable in the cerebrum at birth. However, it is expressed weakly but diffusely in the cerebrum by the fourth day of life. By the 10th day, there is strong expression in the cerebrum, in marked contrast to its virtual absence from the cerebellum at this stage. By quantitative absorption analysis, CNSgp 130 was undetectable on the day of birth, and increased steadily to 80% of adult values by the 22nd day of postnatal life. Binding studies with pure CNSgp 130 demonstrated a Pronase-sensitive ligand in adult chicken brain. This ligand was absent from neonatal rat brain and non-CNS tissues.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09195.x
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  • 97
    Electronic Resource
    Electronic Resource
    Biochemical Aspects of Chick Embryo Retina Development: The Effects of Glucocorticoids (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In chick embryo retina during development, DNA synthesis and the activities of DNA polymerase, thymidine kinase, thymidylate synthetase, and ornithine decarboxylase (ODC) declined in parallel from day 7 to 12. The administration in ovo of hydrocortisone reduced significantly, particularly at 8–10 days of incubation, both DNA synthesis and the four enzyme activities tested. The effect was dose dependent, reaching the maximum with 50–100 nmol of hydrocortisone, 8–16 h after treatment. The highest inhibition was found for ODC activity (70%), followed by thymidine kinase activity (62%) and DNA synthesis (45%), whereas activities of DNA polymerase and thymidylate synthetase were reduced only by 30%. The inhibitory effect was exerted by all the glucocorticoids tested, with dexamethasone and hydrocortisone being the most efficacious. The results support the view that glucocorticoids reduce the proliferative events in chick embryo retina, particularly at 8–10 days of embryonic life.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09198.x
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  • 98
    Electronic Resource
    Electronic Resource
    Dopamine Autoreceptors Modulate the Phosphorylation of Tyrosine Hydroxylase in Rat Striatal Slices (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The hypothesis that dopamine (DA) autoreceptors modulate the phosphorylation of tyrosine hydroxylase (TH; EC 1.14.16.2) was investigated in rat striatal slices. Tissue was prelabeled with 32P inorganic phosphate, and TH recovered by immunoprecipitation with anti-TH rabbit serum. The TH monomer was resolved on sodium dodecyl sulfate polyacrylamide gels, and the extent of phosphorylation was determined by scanning densitometry of autoradiographs. Depolarization of striatal slices with 55 mM K+ markedly increased the incorporation of 32P into several proteins, including the TH monomer (Mr= 60,000). A similar increase in TH phosphorylation occurred in response to the adenylate cyclase activator forskolin and the cyclic AMP analog dibutyryl cyclic AMP. An increase in TH phosphorylation was not observed in response to the D1-selective agonist SKF 38393. The D2-selective DA autoreceptor agonist pergolide decreased the phosphorylation of TH below basal levels and blocked the increase in phosphorylation elicited by 55 mM K+. The inhibitory effect of pergolide was antagonized by the D2-selective antagonist eticlopride. Changes observed in the phosphorylation of TH were mirrored by changes in tyrosine hydroxylation in situ. These observations support the hypothesis that a reduction in TH phosphorylation is the mechanism by which DA autoreceptors modulate tyrosine hydroxylation in nigrostriatal nerve terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09202.x
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  • 99
    Electronic Resource
    Electronic Resource
    Coordinate Regulation of Ganglioside Glycosyltransferases in Differentiating NG108-15 Neuroblastoma X Glioma Cells (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The enzymatic basis for ganglioside regulation during differentiation of NG108-15 mouse neuroblastoma X rat glioma hybrid cells was studied. This cell line contains four gangliosides that lie along the same biosynthetic pathway: GM3, GM2, GM1, and GD1a. Chemically induced neuronal differentiation of NG108-15 cells led to an 80% drop in the steady-state level of their major ganglioside, GM3, a sixfold increase in the level of a minor ganglioside, GM2 (which became the predominant ganglioside of differentiated cells); and relatively little change in the levels of GM1 and GD1a, which lie further along the same biosynthetic pathway. The enzymatic basis for this selective change in ganglioside expression was investigated by measuring the activity of two glycosyltransferases involved in ganglioside biosynthesis. UDP-N-acetylgalactosamine:GM3 N-acetylgalactosaminyltransferase (GM2-synthetase) activity increased fivefold during butyrate-induced differentiation, whereas UDP-galactose: GM2 galactosyltransferase (GM1-synthetase) activity decreased to 10% of its control level. Coordinate regulation of these two glycosyltransferases appears to be primarily responsible for the selective increase of GM2 expression during NG108-15 differentiation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09205.x
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  • 100
    Electronic Resource
    Electronic Resource
    Role of Intracellular pH in the Axolemma- and Myelin-Induced Proliferation of Schwann Cells (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In order to provide additional information on the biochemical events that interact to cause Schwann cells to proliferate, we have monitored the intracellular pH of Schwann cells that have been stimulated to divide with myelin-enriched fractions (MEF) or axolemma-enriched fractions (AEF). The intracellular pH of Schwann cells was monitored using 2′,7′-bis(carboxymethyl)-5(6)-carboxyfluorescein (BCECF), which displays an increase in fluorescence upon alkalinization. Both AEF and MEF caused dose-dependent increases in the intracellular fluorescence of the Schwann cell cultures. At their maximum doses, AEF and MEF stimulation resulted in a 260 and 300% increase in intracellular fluorescence, respectively. The increase in intracellular fluorescence was abolished when cells were stimulated in Na+-free media, suggesting a role for the Na+/H+ exchanger. Mitotic stimulation required integrity of the Na+/H+ exchanger, as inhibition of the Na+/H+ exchanger for periods up to 1 h after addition of mitogen caused a significant inhibition of subsequent mitosis. Phorbol esters, which can potentiate AEF-and MEF-induced Schwann cell proliferation, increased intracellular fluorescence fivefold, an effect which was also dependent upon the presence of Na+ in the culture media. The specificity of the increase in intracellular pH for AEF and MEF was tested by incubating Schwann cells with liver microsomes and a biologically inactive phorbol alcohol, neither of which is significantly mitogenic for Schwann cells. Neither liver microsomes nor phorbol alcohol had a significant effect on intracellular pH. The implications of the increase in intracellular pH in Schwann cells with respect to inositol phospholipid metabolism, protein kinase C activation, and cellular proliferation are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb09211.x
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