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  • 1
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    Comparison of two forms of long-term potentiation in single hippocampal neurons (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-06-29
    Description: In invertebrate nervous systems, some long-lasting increases in synaptic efficacy result from changes in the presynaptic cell. In the vertebrate nervous system, the best understood long-lasting change in synaptic strength is long-term potentiation (LTP) in the CA1 region of the hippocampus. Here the process is initiated postsynaptically, but the site of the persistent change is unresolved. Single CA3 hippocampal pyramidal cells receive excitatory inputs from associational-commissural fibers and from the mossy fibers of dentate granule cells and both pathways exhibit LTP. Although the induction of associational-commissural LTP requires in the postsynaptic cell N-methyl-D-aspartate (NMDA) receptor activation, membrane depolarization, and a rise in calcium, mossy fiber LTP does not. Paired-pulse facilitation, which is an index of increased transmitter release, is unaltered during associational-commissural LTP but is reduced during mossy fiber LTP. Thus, both the induction and the persistent change may be presynaptic in mossy fiber LTP but not in associational-commissural LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zalutsky, R A -- Nicoll, R A -- MH0437/MH/NIMH NIH HHS/ -- MH38256/MH/NIMH NIH HHS/ -- NS24205/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Jun 29;248(4963):1619-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Physiology, University of California, San Francisco, CA 94114-0450.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2114039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Egtazic Acid/pharmacology ; Electric Stimulation ; Evoked Potentials ; Fluorides/pharmacology ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Membrane Potentials/drug effects ; Microelectrodes ; Neurons/drug effects/*physiology ; Synapses/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Mediation of hippocampal mossy fiber long-term potentiation by cyclic AMP (1994)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1994-09-23
    Description: Repetitive activation of hippocampal mossy fibers evokes a long-term potentiation (LTP) of synaptic responses in pyramidal cells in the CA3 region that is independent of N-methyl-D-aspartate receptor activation. Previous results suggest that the site for both the induction and expression of this form of LTP is presynaptic. Experimental elevation of cyclic adenosine 3',5'-monophosphate (cAMP) both mimics and interferes with tetanus-induced mossy fiber LTP, and blockers of the cAMP cascade block mossy fiber LTP. It is proposed that calcium entry into the presynaptic terminal may activate Ca(2+)-calmodulin-sensitive adenylyl cyclase I which, through protein kinase A, causes a persistent enhancement of evoked glutamate release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weisskopf, M G -- Castillo, P E -- Zalutsky, R A -- Nicoll, R A -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1878-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Graduate Program, University of California, San Francisco 94143-0450.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916482" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; *Carbazoles ; Colforsin/pharmacology ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Glutamates/metabolism/pharmacology ; Glutamic Acid ; Guinea Pigs ; Hippocampus/*physiology ; In Vitro Techniques ; Indoles/pharmacology ; Isoquinolines/pharmacology ; *Long-Term Potentiation/drug effects ; Models, Biological ; Nerve Fibers/*physiology ; Presynaptic Terminals/metabolism ; Pyramidal Cells/physiology ; Pyrroles/pharmacology ; *Sulfonamides ; Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Long-term potentiation: evidence against an increase in transmitter release probability in the CA1 region of the hippocampus (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-23
    Description: It is widely accepted that N-methyl-D-aspartate (NMDA)-receptor-dependent long-term potentiation (LTP) in the CA1 region of the hippocampus is triggered postsynaptically, but there is considerable debate as to the site at which the increase in synaptic strength is expressed. The irreversible open-channel blocking action of the NMDA receptor antagonist MK-801 has been used to test whether the probability of transmitter release (Pr) is increased during LTP. Although the rate of decline of the amplitude of the NMDA receptor-mediated excitatory postsynaptic current (EPSC) in the presence of MK-801 strongly depends on Pr, the rate of decline of the EPSC evoked at synapses expressing LTP is identical to that observed at synapses not expressing LTP. These findings are difficult to reconcile with models in which the expression of LTP is due to an increase in Pr.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manabe, T -- Nicoll, R A -- New York, N.Y. -- Science. 1994 Sep 23;265(5180):1888-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dizocilpine Maleate/pharmacology ; Guinea Pigs ; Hippocampus/*metabolism ; In Vitro Techniques ; *Long-Term Potentiation ; Male ; Neurotransmitter Agents/*metabolism ; Receptors, AMPA/antagonists & inhibitors/physiology ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*physiology ; Synapses/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Release of adenosine by activation of NMDA receptors in the hippocampus (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-09-30
    Description: Adenosine is present in the mammalian brain in large amounts and has potent effects on neuronal activity, but its role in neural signaling is poorly understood. The glutamate receptor agonist N-methyl-D-aspartate (NMDA) caused a presynaptic depression of excitatory synaptic transmission in the CA1 region of guinea pig hippocampal slices. This depression was blocked by an adenosine A1 receptor antagonist, which suggests that activation of the NMDA subtype of glutamate receptor raises the concentration of extracellular adenosine, which acts on presynaptic inhibitory A1 receptors. Strong tetanic stimulation caused a heterosynaptic inhibition that was blocked by both NMDA and A1 receptor antagonists. Enkephalin, which selectively inhibits interneurons, antagonized the heterosynaptic inhibition. These findings suggest that synaptically released glutamate activates NMDA receptors, which in turn releases adenosine, at least in part from interneurons, that acts at a distance to inhibit presynaptically the release of glutamate from excitatory synapses. Thus, interneurons may mediate a widespread purinergic presynaptic inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manzoni, O J -- Manabe, T -- Nicoll, R A -- New York, N.Y. -- Science. 1994 Sep 30;265(5181):2098-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California at San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7916485" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Adenosine/*metabolism ; Animals ; Electric Stimulation ; Enkephalins/pharmacology ; GABA-B Receptor Antagonists ; Glutamates/metabolism ; Glutamic Acid ; Guinea Pigs ; Hippocampus/drug effects/*metabolism ; In Vitro Techniques ; Interneurons/drug effects/*metabolism ; Male ; N-Methylaspartate/pharmacology ; Neural Inhibition/drug effects ; Organophosphorus Compounds/pharmacology ; Receptors, N-Methyl-D-Aspartate/drug effects/*metabolism ; Synapses/*metabolism ; Synaptic Transmission/drug effects ; Theophylline/analogs & derivatives/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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