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  • 1
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1996-03-01
    Beschreibung: Analysis of strontium-induced asynchronous release of quanta from stimulated synapses revealed that long-term potentiation and long-term depression in the CA1 region of the mammalian hippocampus are associated with an increase and a decrease, respectively, in quantal size. At a single set of synapses, the increase in quantal size seen with long-term potentiation was completely reversed by depotentiating stimuli. Long-term potentiation and depression are also associated with an increase and decrease, respectively, in the frequency of quantal events, consistent with an all-or-none regulation (up or down) of clusters of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, a change in the release of transmitter, or both.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oliet, S H -- Malenka, R C -- Nicoll, R A -- New York, N.Y. -- Science. 1996 Mar 1;271(5253):1294-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco 94143-0450, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638114" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcium/pharmacology ; Electric Stimulation ; Evoked Potentials ; Guinea Pigs ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Long-Term Potentiation/*physiology ; Neuronal Plasticity/*physiology ; Neurons/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/physiology ; Strontium/pharmacology ; Synapses/*physiology ; *Synaptic Transmission
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1993-08-20
    Beschreibung: The effectiveness of long-term potentiation (LTP) as a mechanism for information storage would be severely limited if processes that decrease synaptic strength did not also exist. In area CA1 of the rat hippocampus, prolonged periods of low-frequency afferent stimulation elicit a long-term depression (LTD) that is specific to the stimulated input. The induction of LTD was blocked by the extracellular application of okadaic acid or calyculin A, two inhibitors of protein phosphatases 1 and 2A. The loading of CA1 cells with microcystin LR, a membrane-impermeable protein phosphatase inhibitor, or calmodulin antagonists also blocked or attenuated LTD. The application of calyculin A after the induction of LTD reversed the synaptic depression, suggesting that phosphatase activity is required for the maintenance of LTD. These findings indicate that the synaptic activation of protein phosphatases plays an important role in the regulation of synaptic transmission.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mulkey, R M -- Herron, C E -- Malenka, R C -- MH00942/MH/NIMH NIH HHS/ -- MH10306/MH/NIMH NIH HHS/ -- MH45334/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1993 Aug 20;261(5124):1051-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of California, San Francisco 94143-0984.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8394601" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Calcium/metabolism ; Calmodulin/metabolism ; Electric Stimulation ; Ethers, Cyclic/pharmacology ; Hippocampus/drug effects/enzymology/*physiology ; Microcystins ; Okadaic Acid ; Oxazoles/pharmacology ; Peptides, Cyclic/pharmacology ; Phosphoprotein Phosphatases/antagonists & inhibitors/*metabolism ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/physiology ; Synapses/drug effects/*physiology ; *Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1992-02-07
    Beschreibung: Long-term potentiation (LTP) is an extensively studied model of synaptic plasticity, in part because it is a plausible biological correlate for the Hebbian synaptic modification that forms the basis for theoretical models of neural development, learning, and memory. Although these models must incorporate algorithms that constrain synaptic weight changes, physiological evidence for such mechanisms is limited. Examination of LTP in area CA1 of the hippocampus revealed that the threshold for LTP induction was not fixed but could be strongly influenced by the recent history of synaptic activity. This effect was transient, synapse-specific, and dependent on postsynaptic N-methyl-D-aspartate (NMDA) receptor activation. These results suggest that the threshold for LTP induction may be continually adjusted according to the recent history of NMDA receptor activation and provide a physiological mechanism by which LTP can be transiently inhibited.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Y Y -- Colino, A -- Selig, D K -- Malenka, R C -- MH00942/MH/NIMH NIH HHS/ -- MH45334/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1992 Feb 7;255(5045):730-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1346729" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): 2-Amino-5-phosphonovalerate/pharmacology ; Action Potentials/drug effects ; Animals ; Electric Stimulation ; Electrophysiology ; Hippocampus/*physiology ; N-Methylaspartate/pharmacology ; Neuronal Plasticity ; Rats ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/physiology ; Synapses/drug effects/*physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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