The life cycle of Ca(2+) ions in dendritic spines

Neuron. 2002 Jan 31;33(3):439-52. doi: 10.1016/s0896-6273(02)00573-1.


Spine Ca(2+) is critical for the induction of synaptic plasticity, but the factors that control Ca(2+) handling in dendritic spines under physiological conditions are largely unknown. We studied [Ca(2+)] signaling in dendritic spines of CA1 pyramidal neurons and find that spines are specialized structures with low endogenous Ca(2+) buffer capacity that allows large and extremely rapid [Ca(2+)] changes. Under physiological conditions, Ca(2+) diffusion across the spine neck is negligible, and the spine head functions as a separate compartment on long time scales, allowing localized Ca(2+) buildup during trains of synaptic stimuli. Furthermore, the kinetics of Ca(2+) sources governs the time course of [Ca(2+)] signals and may explain the selective activation of long-term synaptic potentiation (LTP) and long-term depression (LTD) by NMDA-R-mediated synaptic Ca(2+).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials / physiology
  • Animals
  • Bicuculline / pharmacology
  • Buffers
  • Calcium / metabolism*
  • Cells, Cultured
  • Dendrites / metabolism*
  • Excitatory Amino Acid Antagonists / pharmacology
  • Fluorescent Dyes / metabolism
  • GABA Antagonists / pharmacology
  • Hippocampus / cytology
  • Hippocampus / metabolism*
  • In Vitro Techniques
  • Mathematics
  • Microscopy, Confocal
  • Models, Neurological
  • Neurons / cytology
  • Neurons / drug effects
  • Neurons / metabolism*
  • Quinoxalines / pharmacology
  • Rats
  • Receptors, N-Methyl-D-Aspartate / metabolism


  • Buffers
  • Excitatory Amino Acid Antagonists
  • Fluorescent Dyes
  • GABA Antagonists
  • Quinoxalines
  • Receptors, N-Methyl-D-Aspartate
  • 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline
  • Calcium
  • Bicuculline