The role of alpha-CaMKII autophosphorylation in neocortical experience-dependent plasticity

Nat Neurosci. 2000 Sep;3(9):911-8. doi: 10.1038/78820.

Abstract

Calcium/calmodulin kinase type II (CaMKII) is a major postsynaptic density protein. CaMKII is postulated to act as a 'molecular switch', which, when triggered by a transient rise in calcium influx, becomes active for prolonged periods because of its ability to autophosphorylate. We studied experience-dependent plasticity in the barrel cortex of mice carrying a point mutation of the alpha-CaMKII gene (T286A), which abolishes this enzyme's ability to autophosphorylate. Plasticity was prevented in adult and adolescent mice homozygous for the mutation, but was normal in heterozygotes and wild-type littermates. These results provide evidence that the molecular switch hypothesis is valid for neocortical experience-dependent plasticity.

Publication types

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

MeSH terms

  • Age Factors
  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Calcium-Calmodulin-Dependent Protein Kinases / deficiency*
  • Calcium-Calmodulin-Dependent Protein Kinases / genetics
  • Heterozygote
  • Learning / physiology*
  • Mechanoreceptors / cytology
  • Mechanoreceptors / metabolism
  • Mice
  • Mice, Knockout
  • Neocortex / cytology
  • Neocortex / growth & development
  • Neocortex / metabolism*
  • Neuronal Plasticity / physiology*
  • Neurons / cytology
  • Neurons / metabolism*
  • Phosphorylation
  • Point Mutation / physiology
  • Somatosensory Cortex / cytology
  • Somatosensory Cortex / growth & development
  • Somatosensory Cortex / metabolism
  • Synapses / metabolism*
  • Synapses / ultrastructure
  • Vibrissae / innervation
  • Vibrissae / physiology

Substances

  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Calcium-Calmodulin-Dependent Protein Kinases