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PubMed · 10395573

Calcium- and activity-dependent synaptic plasticity.

R S Zucker
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Abstract

Calcium ions play crucial signaling roles in many forms of activity-dependent synaptic plasticity. Recent presynaptic [Ca2+]i measurements and manipulation of presynaptic exogenous buffers reveal roles for residual [Ca2+]i following conditioning stimulation in all phases of short-term synaptic enhancement. Pharmacological manipulations implicate mitochondria in post-tetanic potentiation. New evidence supports an influence of Ca2+ in replacing depleted vesicles after synaptic depression. In addition, high-resolution measurements of [Ca2+]i in dendritic spines show how Ca2+ can encode the precise relative timing of presynaptic input and postsynaptic activity and generate long-term synaptic modifications of opposite polarity.

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AnimalsCalciumCalcium SignalingNeuronal PlasticityNeuronsJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.Review

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R S Zucker. 1999. Calcium- and activity-dependent synaptic plasticity.. https://doi.org/10.1016/s0959-4388(99)80045-2

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