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Brief Communication
Nature Neuroscience  5, 295 - 296 (2002)
Published online: 26 March 2002; | doi:10.1038/nn829

Protein kinase Mzeta is necessary and sufficient for LTP maintenance

Douglas S.F. Ling, Larry S. Benardo, Peter A. Serrano, Nancy Blace, Matthew T. Kelly, John F. Crary & Todd C. Sacktor

Departments of Physiology, Pharmacology, and Neurology, SUNY Downstate Medical Center, 450 Clarkson Ave., Brooklyn, New York, 11203, USA

Correspondence should be addressed to Todd C. Sacktor tsacktor@downstate.edu
Long-term potentiation (LTP), a persistent synaptic enhancement thought to be a substrate for memory1, can be divided into two phases: induction, triggering potentiation, and maintenance, sustaining it over time1, 2. Many postsynaptic events are implicated in induction, including N-methyl-D-aspartate receptor (NMDAR) activation, calcium increases and stimulation of several protein kinases1; in contrast, the mechanism maintaining LTP is not yet characterized1. Here we show the constitutively active form of an atypical protein kinase C (PKC) isozyme, protein kinase M zeta (PKMzeta), is necessary and sufficient for LTP maintenance.


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Nature Neuroscience
ISSN: 1097-6256
EISSN: 1546-1726
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