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