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4 - Long-term potentiation and long-term depression

from Section A1 - Cellular and molecular mechanisms of neural plasticity

Published online by Cambridge University Press:  05 March 2012

Zafir I. Bashir
Affiliation:
Department of Anatomy, MRC Centre for Synaptic Plasticity, University of Bristol, Bristol, UK
Peter V. Massey
Affiliation:
Department of Anatomy, MRC Centre for Synaptic Plasticity, University of Bristol, Bristol, UK
Michael Selzer
Affiliation:
University of Pennsylvania
Stephanie Clarke
Affiliation:
Université de Lausanne, Switzerland
Leonardo Cohen
Affiliation:
National Institute of Mental Health, Bethesda, Maryland
Pamela Duncan
Affiliation:
University of Florida
Fred Gage
Affiliation:
Salk Institute for Biological Studies, San Diego
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Summary

This chapter concentrates on the basic mechanisms that are thought to underlie induction and expression of long-term plasticity (LTP). LTP has been demonstrated at all of the major synapses in the hippocampus. Activity-dependent LTP is a commonly observed feature of the neocortex and does not differ from the hippocampus in its induction or expression mechanisms. The induction and/or the magnitude of LTP and long-term depression (LTD) can be affected by prior activity that in itself does not produce observable changes in synaptic efficacy. Thus there is some plastic change of a different, or meta, form that influences traditional synaptic plasticity. N-methyl-D-aspartate receptors (NMDAR)-mediated synaptic transmission can undergo potentiation and depression, and given the critical role for NMDARs in LTP and LTD induction it is apparent that any change in NMDAR synaptic transmission brought about by a priming stimulus could have dramatic consequences for induction of LTP and LTD.
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Publisher: Cambridge University Press
Print publication year: 2006

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