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Calcium stores regulate the polarity and input specificity of synaptic modification

Calcium stores regulate the polarity and input specificity of synaptic modification Activity-induced synaptic modification is essential for the development and plasticity of the nervous system 1,2,3 . Repetitive correlated activation of pre- and postsynaptic neurons can induce persistent enhancement or decrement of synaptic efficacy, commonly referred to as long-term potentiation or depression 2,3 (LTP or LTD). An important unresolved issue is whether and to what extent LTP and LTD are restricted to the activated synapses 4,5,6,7,8 . Here we show that, in the CA1 region of the hippocampus, reduction of postsynaptic calcium influx by partial blockade of NMDA (N-methyl-d-aspartate) receptors results in a conversion of LTP to LTD and a loss of input specificity normally associated with LTP, with LTD appearing at heterosynaptic inputs. The induction of LTD at homo- and heterosynaptic sites requires functional ryanodine receptors and inositol triphosphate (InsP3) receptors, respectively. Functional blockade or genetic deletion of type 1 InsP3 receptors led to a conversion of LTD to LTP and elimination of heterosynaptic LTD, whereas blocking ryanodine receptors eliminated only homosynaptic LTD. Thus, postsynaptic Ca2+, deriving from Ca2+ influx and differential release of Ca2+ from internal stores through ryanodine and InsP3 receptors, regulates both the polarity and input specificity of activity-induced synaptic modification. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Springer Journals

Calcium stores regulate the polarity and input specificity of synaptic modification

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References (38)

Publisher
Springer Journals
Copyright
Copyright © 2000 by Macmillan Magazines Ltd.
Subject
Science, Humanities and Social Sciences, multidisciplinary; Science, Humanities and Social Sciences, multidisciplinary; Science, multidisciplinary
ISSN
0028-0836
eISSN
1476-4687
DOI
10.1038/35046067
Publisher site
See Article on Publisher Site

Abstract

Activity-induced synaptic modification is essential for the development and plasticity of the nervous system 1,2,3 . Repetitive correlated activation of pre- and postsynaptic neurons can induce persistent enhancement or decrement of synaptic efficacy, commonly referred to as long-term potentiation or depression 2,3 (LTP or LTD). An important unresolved issue is whether and to what extent LTP and LTD are restricted to the activated synapses 4,5,6,7,8 . Here we show that, in the CA1 region of the hippocampus, reduction of postsynaptic calcium influx by partial blockade of NMDA (N-methyl-d-aspartate) receptors results in a conversion of LTP to LTD and a loss of input specificity normally associated with LTP, with LTD appearing at heterosynaptic inputs. The induction of LTD at homo- and heterosynaptic sites requires functional ryanodine receptors and inositol triphosphate (InsP3) receptors, respectively. Functional blockade or genetic deletion of type 1 InsP3 receptors led to a conversion of LTD to LTP and elimination of heterosynaptic LTD, whereas blocking ryanodine receptors eliminated only homosynaptic LTD. Thus, postsynaptic Ca2+, deriving from Ca2+ influx and differential release of Ca2+ from internal stores through ryanodine and InsP3 receptors, regulates both the polarity and input specificity of activity-induced synaptic modification.

Journal

Nature – Springer Journals

Published: Nov 30, 2000

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