Dendritic spine formation and pruning: common cellular mechanisms?

Trends Neurosci. 2000 Feb;23(2):53-7. doi: 10.1016/s0166-2236(99)01499-x.


The recent advent of novel high-resolution imaging methods has created a flurry of exciting observations that address a century-old question: what are biological signals that regulate formation and elimination of dendritic spines? Contrary to the traditional belief that the spine is a stable storage site of long-term neuronal memory, the emerging picture is of a dynamic structure that can undergo fast morphological variations. Recent conflicting reports on the regulation of spine morphology lead to the proposal of a unifying hypothesis for a common mechanism involving changes in postsynaptic intracellular Ca2+ concentration, [Ca2+]i: a moderate rise in [Ca2+]i causes elongation of dendritic spines, while a very large increase in [Ca2+]i causes fast shrinkage and eventual collapse of spines. This hypothesis provides a parsimonious explanation for conflicting reports on activity-dependent changes in dendritic spine morphology, and might link these changes to functional plasticity in central neurons.

Publication types

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

MeSH terms

  • Animals
  • Calcium / metabolism
  • Cell Culture Techniques
  • Cell Size
  • Dendrites / metabolism*
  • Humans
  • Models, Biological
  • Neuronal Plasticity
  • Signal Transduction


  • Calcium