CaMKII Regulation in Information Processing and Storage

Trends Neurosci. 2012 Oct;35(10):607-18. doi: 10.1016/j.tins.2012.05.003. Epub 2012 Jun 19.

Abstract

The Ca(2+)/Calmodulin(CaM)-dependent protein kinase II (CaMKII) is activated by Ca(2+)/CaM, but becomes partially autonomous (Ca(2+)-independent) upon autophosphorylation at T286. This hallmark feature of CaMKII regulation provides a form of molecular memory and is indeed important in long-term potentiation (LTP) of excitatory synapse strength and memory formation. However, emerging evidence supports a direct role in information processing, while storage of synaptic information may instead be mediated by regulated interaction of CaMKII with the NMDA receptor (NMDAR) complex. These and other CaMKII regulation mechanisms are discussed here in the context of the kinase structure and their impact on postsynaptic functions. Recent findings also implicate CaMKII in long-term depression (LTD), as well as functional roles at inhibitory synapses, lending renewed emphasis on better understanding the spatiotemporal control of CaMKII regulation.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism*
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / physiology*
  • Gene Expression Regulation, Enzymologic / physiology
  • Hippocampus / metabolism
  • Hippocampus / physiology
  • Humans
  • Isoenzymes / metabolism
  • Long-Term Potentiation / physiology
  • Long-Term Synaptic Depression / physiology
  • Memory / physiology*
  • Neural Inhibition / physiology
  • Phosphorylation
  • Protein Conformation
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Receptors, N-Methyl-D-Aspartate / physiology
  • Synapses / metabolism
  • Synapses / physiology*
  • Synaptic Transmission / physiology*

Substances

  • Isoenzymes
  • Receptors, N-Methyl-D-Aspartate
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2