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  • 1
    Publication Date: 1988-10-07
    Description: Brief repetitive activation of excitatory synapses in the hippocampus leads to an increase in synaptic strength that lasts for many hours. This long-term potentiation (LTP) of synaptic transmission is the most compelling cellular model in the vertebrate brain for learning and memory. The critical role of postsynaptic calcium in triggering LTP has been directly examined using three types of experiment. First, nitr-5, a photolabile nitrobenzhydrol tetracarboxylate calcium chelator, which releases calcium in response to ultraviolet light, was used. Photolysis of nitr-5 injected into hippocampal CA1 pyramidal cells resulted in a large enhancement of synaptic transmission. Second, in agreement with previous results, buffering intracellular calcium at low concentrations blocked LTP. Third, depolarization of the postsynaptic membrane so that calcium entry is suppressed prevented LTP. Taken together, these results demonstrate that an increase in postsynaptic calcium is necessary to induce LTP and sufficient to potentiate synaptic transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malenka, R C -- Kauer, J A -- Zucker, R S -- Nicoll, R A -- MH00437/MH/NIMH NIH HHS/ -- MH38256/MH/NIMH NIH HHS/ -- NS24205/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 Oct 7;242(4875):81-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2845577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology ; Chelating Agents/pharmacology ; Egtazic Acid/analogs & derivatives/pharmacology ; Evoked Potentials/drug effects ; Hippocampus/*physiology ; In Vitro Techniques ; Kinetics ; Photolysis ; Pyramidal Tracts/physiology ; Rats ; Synapses/*physiology ; *Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 1986-12-05
    Description: Both serotonin and the selective gamma-aminobutyric acidB (GABAB) agonist, baclofen, increase potassium (K+) conductance in hippocampal pyramidal cells. Although these agonists act on separate receptors, the potassium currents evoked by the agonists are not additive, indicating that the two receptors share the same potassium channels. Experiments with hydrolysis-resistant guanosine triphosphate (GTP) and guanosine diphosphate analogs and pertussis toxin indicate that the opening of the potassium channels by serotonin and GABAB receptors involves a pertussis toxin-sensitive GTP-binding (G) protein, which may directly couple the two receptors to the potassium channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andrade, R -- Malenka, R C -- Nicoll, R A -- MH38256/MH/NIMH NIH HHS/ -- MN00437/MN/OMHHE CDC HHS/ -- NS07495/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1261-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2430334" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Baclofen/pharmacology ; Calcium/metabolism ; GTP-Binding Proteins/*pharmacology ; Guanosine 5'-O-(3-Thiotriphosphate) ; Guanosine Diphosphate/analogs & derivatives/pharmacology ; Guanosine Triphosphate/analogs & derivatives/pharmacology ; Hippocampus/*drug effects ; Ion Channels/*metabolism ; Phorbol 12,13-Dibutyrate ; Phorbol Esters/pharmacology ; Potassium/metabolism ; Rats ; Receptors, GABA-A/*drug effects/metabolism ; Receptors, Serotonin/*drug effects/metabolism ; Serotonin/pharmacology ; Spiperone/pharmacology ; Thionucleotides/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 568 (1989), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 4
    Publication Date: 1986-12-05
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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