Plasticity of calcium channels in dendritic spines

Nat Neurosci. 2003 Sep;6(9):948-55. doi: 10.1038/nn1112.


Voltage-sensitive Ca2+ channels (VSCCs) constitute a major source of calcium ions in dendritic spines, but their function is unknown. Here we show that R-type VSCCs in spines of rat CA1 pyramidal neurons are depressed for at least 30 min after brief trains of back-propagating action potentials. Populations of channels in single spines are depressed stochastically and synchronously, independent of channels in the parent dendrite and other spines, implying that depression is the result of signaling restricted to individual spines. Induction of VSCC depression blocks theta-burst-induced long-term potentiation (LTP), indicating that postsynaptic action potentials can modulate synaptic plasticity by tuning VSCCs. Induction of depression requires [Ca2+] elevations and activation of L-type VSCCs, which activate Ca2+/calmodulin-dependent kinase II (CaMKII) and a cyclic adenosine monophosphate (cAMP)-dependent pathway. Given that L-type VSCCs do not contribute measurably to Ca2+ influx in spines, they must activate downstream effectors either directly through voltage-dependent conformational changes or via [Ca2+] microdomains.

Publication types

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

MeSH terms

  • Action Potentials / drug effects
  • Action Potentials / physiology*
  • Animals
  • Calcium / pharmacology
  • Calcium / physiology
  • Calcium Channels, R-Type / physiology*
  • Dendrites / drug effects
  • Dendrites / physiology*
  • Hippocampus / cytology
  • Hippocampus / drug effects
  • Hippocampus / physiology
  • In Vitro Techniques
  • Neuronal Plasticity / drug effects
  • Neuronal Plasticity / physiology*
  • Rats


  • Calcium Channels, R-Type
  • Calcium