Calcium- and activity-dependent synaptic plasticity

Curr Opin Neurobiol. 1999 Jun;9(3):305-13. doi: 10.1016/s0959-4388(99)80045-2.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Calcium / physiology*
  • Calcium Signaling / physiology*
  • Neuronal Plasticity / physiology*
  • Neurons / physiology*


  • Calcium