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
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 |
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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: | https://repository.cshl.edu/id/eprint/28736 |
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