Synaptic Plasticity and Memory Function

Abstract

Research was conducted to test the hypothesis that activation of the calcium-dependent protease, calpain, is involved in the induction of long-term potentiation (LTP) of synaptic transmission and memory storage in the mammalian brain. Evidence indicates that naturally-occurring patterns of synaptic activity can induce LTP by activating an NMDA receptor that allows postsynaptic influx of calcium. Activation of NMDA receptors induces a calcium-dependent proteolysis of spectrin, a calpain substrate; both calpain and spectrin are present in dendritic spines. Both a calpain inhibitor and a NMDA receptor antagonist have been found to interfere with spatial and olfactory learning. Calpain-mediated spectrin degradation occurs in vivo after various treatments, studies of simple cell types suggest that this mechanism may produce structural changes similar to those which accompany LTP. Keywords: Learning, Memory, Long term Potentiation, Calpain brain spectrin, Olfactory learning.

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Document Details

Document Type
Technical Report
Publication Date
May 24, 1988
Accession Number
ADA198473

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  • Gary Lynch

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  • University of California, Irvine

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  • Biology

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