The molecular basis of CaMKII function in synaptic and behavioural memory

Lisman, J., Schulman, H., Cline, H. (March 2002) The molecular basis of CaMKII function in synaptic and behavioural memory. Nature Reviews Neuroscience, 3 (3). pp. 175-190. ISSN 1471-0048

URL: http://www.ncbi.nlm.nih.gov/pubmed/11994750
DOI: 10.1038/nrn753

Abstract

Long-term potentiation (LTP) in the CA1 region of the hippocampus has been the primary model by which to study the cellular and molecular basis of memory. Calcium/calmodulin-dependent protein kinase II (CaMKII) is necessary for LTP induction, is persistently activated by stimuli that elicit LTP, and can, by itself, enhance the efficacy of synaptic transmission. The analysis of CaMKII autophosphorylation and dephosphorylation indicates that this kinase could serve as a molecular switch that is capable of long-term memory storage. Consistent with such a role, mutations that prevent persistent activation of CaMKII block LTP, experience-dependent plasticity and behavioural memory. These results make CaMKII a leading candidate in the search for the molecular basis of memory.

Item Type: Paper
Subjects: bioinformatics > genomics and proteomics > genetics & nucleic acid processing > protein structure, function, modification > protein types > enzymes > kinase > CaMKII
bioinformatics > genomics and proteomics > genetics & nucleic acid processing > protein structure, function, modification > protein types > enzymes > kinase
organism description > animal behavior > memory
organs, tissues, organelles, cell types and functions > cell types and functions > cell functions > synaptic transmission
CSHL Authors:
Communities: CSHL labs > Cline lab
Depositing User: Matt Covey
Date: March 2002
Date Deposited: 08 Jan 2014 15:48
Last Modified: 08 Jan 2014 15:48
Related URLs:
URI: http://repository.cshl.edu/id/eprint/28736

Actions (login required)

Administrator's edit/view item Administrator's edit/view item
CSHL HomeAbout CSHLResearchEducationNews & FeaturesCampus & Public EventsCareersGiving