Molecular memory by reversible translocation of calcium/calmodulin-dependent protein kinase II.

Published

Journal Article

Synaptic plasticity is thought to be a key process for learning, memory and other cognitive functions of the nervous system. The initial events of plasticity require the conversion of brief electrical signals into alterations of the biochemical properties of synapses that last for much longer than the initial stimuli. Here we show that a regulator of synaptic plasticity, calcium/calmodulin-dependent protein kinase IIalpha (CaMKII), sequentially translocates to postsynaptic sites, undergoes autophosphorylation and gets trapped for several minutes until its dissociation is induced by secondary autophosphorylation and phosphatase 1 action. Once dissociated, CaMKII shows facilitated translocation for several minutes. This suggests that trapping of CaMKII by its targets and priming of CaMKII translocation may function as biochemical memory mechanisms that change the signaling capacity of synapses.

Full Text

Duke Authors

Cited Authors

  • Shen, K; Teruel, MN; Connor, JH; Shenolikar, S; Meyer, T

Published Date

  • September 2000

Published In

Volume / Issue

  • 3 / 9

Start / End Page

  • 881 - 886

PubMed ID

  • 10966618

Pubmed Central ID

  • 10966618

International Standard Serial Number (ISSN)

  • 1097-6256

Digital Object Identifier (DOI)

  • 10.1038/78783

Language

  • eng

Conference Location

  • United States