Calcium- and activity-dependent synaptic plasticity.
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.
Department of Molecular and Cell Biology, University of California (Berkeley), 111 Life Sciences Addition, Berkeley, California 94720-3200, USA. zucker@socrates.berkeley.edu
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D000818:Animals; D002118:Calcium / Q000502:physiology*; D020013:Calcium Signaling / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology*
D002118:Calcium