Publication Date:
1988-11-04
Description:
Long-term synaptic potentiation (LTP) is a leading candidate for a synaptic mechanism of rapid learning in mammals. LTP is a persistent increase in synaptic efficacy that can be quickly induced. The biophysical process that controls one type of LTP is formally similar to a synaptic memory mechanism postulated decades ago by the psychologist Donald Hebb. A key aspect of the modification process involves the N-methyl-D-aspartate (NMDA) receptor-ionophore complex. This ionophore allows calcium influx only if the endogenous ligand glutamate binds to the NMDA receptor and if the voltage across the associated channel is also sufficiently depolarized to relieve a magnesium block. According to one popular hypothesis, the resulting increase in the intracellular calcium concentration activates protein kinases that enhance the postsynaptic conductance. Further biophysical and molecular understanding of the modification process should facilitate detailed explorations of the mnemonic functions of LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, T H -- Chapman, P F -- Kairiss, E W -- Keenan, C L -- New York, N.Y. -- Science. 1988 Nov 4;242(4879):724-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Yale University, New Haven, CT 06520.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2903551" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
In Vitro Techniques
;
Learning/*physiology
;
Neuronal Plasticity
;
Neurotransmitter Agents/physiology
;
Receptors, Neurotransmitter/physiology
;
Synapses/*physiology
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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