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Nat Rev Neurosci. 2012 Feb 15;13(3):169-82. doi: 10.1038/nrn3192.

Mechanisms of CaMKII action in long-term potentiation.

Author information

1
Department of Biology, Brandeis University, Waltham, Massachusetts 02454, USA. lisman@brandeis.edu

Abstract

Long-term potentiation (LTP) of synaptic strength occurs during learning and can last for long periods, making it a probable mechanism for memory storage. LTP induction results in calcium entry, which activates calcium/calmodulin-dependent protein kinase II (CaMKII). CaMKII subsequently translocates to the synapse, where it binds to NMDA-type glutamate receptors and produces potentiation by phosphorylating principal and auxiliary subunits of AMPA-type glutamate receptors. These processes are all localized to stimulated spines and account for the synapse-specificity of LTP. In the later stages of LTP, CaMKII has a structural role in enlarging and strengthening the synapse.

PMID:
22334212
PMCID:
PMC4050655
DOI:
10.1038/nrn3192
[Indexed for MEDLINE]
Free PMC Article

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