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  • 1
    Electronic Resource
    Electronic Resource
    Hippocampal noradrenergic responses in vivo and in vitro (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 318 (1982), S. 259-266 
    Details
    ISSN: 1432-1912
    Keywords: Norepinephrine ; Alpha receptors ; Beta receptors ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Pressure ejection of l-norepinephrine (NE) in the in vivo rat hippocampus generally produced depression of pyramidal cell spontaneous activity. In addition, both excitation and biphasic responses were observed. NE-induced inhibition of firing rate was effectively antagonized by concurrent administration of the alpha antagonist phentolamine, but was largely unaltered by the beta antagonist timolol. On the other hand, NE-induced elevation in spontaneous firing rate was effectively blocked by timolol, and largely unaffected by phentolamine. Another beta antagonist, sotalol, did not selectively antagonize either NE-induced inhibition or NE-induced excitation. The beta agonist 2-fluoro-NE produced increases in pyramidal cell firing rates in most cells studied, while the alpha agonist 6-fluoro-NE inhibited the majority of cells examined. The effects of sotalol were also examined on alpha and beta receptor-mediated field responses in the in vitro hippocampal slice. Sotalol was shown to be a selective beta antagonist in this system, blocking excitation evoked by the beta agonist isoproterenol while having no effect on inhibition elicited by the alpha agonist clonidine; however, the potency of sotalol (K i=3.5μM) was considerably less than that of timolol (K i=50 nM). Taken together, these results suggest that NE-induced depression and elevation in hippocampal pyramidal cell spontaneous discharge in vivo are mediated via alpha and beta adrenoceptors, respectively.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501163
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Peptide toxins isolated from spider venom that modulate gating of voltage-dependent K+ channels (1999)
    Springer
    Perspectives in drug discovery and design 15-16 (1999), S. 71-81 
    Details
    ISSN: 1573-9023
    Keywords: K channels ; Kv2.1 ; Kv4.2 ; spider ; toxins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Spider venom, like snake, bee and scorpion venom, is a rich source of ion channel modulators. Spider toxins that block Ca2+ channels and glutamate receptor-operated channels have been described. Recently, two new families of toxins that block K+ channels were isolated from spider venom. Hanatoxins, isolated from the venom of the Chilean tarantula Grammostola spatulata, inhibit Kv2.1 and Kv4.2. Kv2.1 is a Shab-related voltage activated K+ channel isolated from rat brain; Kv4.2 is a Shal-related K+ channel responsible for the transient outward K+ current (Ito) that initiates repolarization of cardiac and neural action potentials. Three toxins (heteropodotoxins) isolated from the venom of a free-living spider, Heteropoda venatoria, also inhibit Kv4.2. Because spider venom is logistically difficult to obtain, much less is known about spider venoms than snake and scorpion venoms. It is likely that development of this resource in reserve will yield many more interesting and useful ion channel modulators.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1017091402116
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  • 3
    Electronic Resource
    Electronic Resource
    Electrophysiological actions of somatostatin (SRIF) in hippocampus: Anin vitro study (1986)
    Springer
    Cellular and molecular neurobiology 6 (1986), S. 363-379 
    Details
    ISSN: 1573-6830
    Keywords: somatostatin ; hippocampal slice ; excitation ; local circuit neurons ; interneurons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. The electrophysiological actions of somatostatin (somatotropin release inhibiting factor; SRIF) were investigated in thein vitro hippocampal slice preparation. Intracellular recordings were obtained from pyramidal neurons in area CA1 in slices of hippocampus from guinea pigs and rabbits. 2. Somatostatin, applied via micropressure ejection to CA1 pyramidal-cell somata, was primarily excitatory. The effects, however, were quite variable, with nearly all cells displaying pronounced tachyphylaxis. A majority of cells was depolarized by SRIF, but hyperpolarizations or biphasic depolarization/hyperpolarization responses were also recorded. Only minimal conductance changes were associated with the SRIF-induced voltage changes. 3. Depletion of SRIF, by injection of the intact animal with cysteamine several hours before preparing slices, resulted in no obvious abnormalities in hippocampal slice electrophysiology. 4. Our results obtained with application of exogenous SRIF are consistent with the concept that SRIF acts as an excitatory neurotransmitter/neuromodulator in hippocampus. However, our attempts to demonstrate endogenous SRIF action have thus far been unsuccessful.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00711406
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  • 4
    Electronic Resource
    Electronic Resource
    Design, Synthesis, and Biological Evaluation of Spider Toxin (Argiotoxin-636) Analogs as NMDA Receptor Antagonists (1998)
    Springer
    Pharmaceutical research 15 (1998), S. 31-38 
    Details
    ISSN: 1573-904X
    Keywords: glutamate ; NMDA ; N-methyl-D-aspartate ; Argiotoxin-636 ; Arg-636 ; polyamine spider toxins ; Araxin™ compounds ; ischemic stroke
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Purpose. Twelve synthetic spider toxin analogs were prepared in an effort to better understand the structure-activity relationships of the polyamine portion of argiotoxin-636 (Arg-636), a noncompetitive NMDA receptor (NMDAR) antagonist. Methods. The l,13-diamino-4,8-diazatridecane portion of the side chain of Arg-636 was systematically modified in an effort to further our knowledge of the structural requirements for the alkyl linker spacing between the amine nitrogens. Systematic isosteric replacement of each of the amine nitrogens in the polyamine moiety with either oxygen or carbon provided a series of compounds which were evaluated in vitro for NMDAR antagonist activity. Results. One-half of the heteroatoms found in Arg-636 were removed to provide analogs which maintained in vitro potency below 1 μM. However, these simplified analogs produced similar or more pronounced effects on the cardiovascular system than Arg-636 in vivo. Conclusions. In this set of analogs, a minimum of three basic nitrogens in the side chain was required for maximum potency as NMDAR antagonists. Isosteric nitrogen substitutions in the polyamine chain reduced the in vitro potency of these analogs. An analog binding-conformation model was proposed to rationalize the inactivity of these isosterically substituted analogs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1011988317683
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    Paper (German National Licenses)
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