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Sci. Signal., 9 March 2010
Vol. 3, Issue 112, p. pe9
[DOI: 10.1126/scisignal.3112pe9]

PERSPECTIVES

PINing for Things Past

Todd Charlton Sacktor*

Departments of Physiology, Pharmacology, and Neurology, Robert F. Furchgott Center for Neural and Behavioral Science, State University of New York, Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA.

Abstract: Long-term memories are thought to be maintained by persistent changes in the strength of synaptic connections among neurons, but how such changes can persist for days to years has been one of the fundamental enigmas of neuroscience. Recently, however, one mechanism that is dependent on the persistent increased activity of an enzyme has been shown to be necessary for the persistence of long-term memory. The transient inhibition of the brain-specific, constitutively active protein kinase C isoform PKM{zeta} erases memories that are even months old. This finding raises a number of issues; chief among them is the question, how can PKM{zeta} maintain memories for months when its half-life is probably much shorter? New data suggest how the high abundance of PKM{zeta} can be maintained over long periods of time. The synthesis of PKM{zeta} is inhibited by Pin1 (protein interacting with NIMA 1), a peptidyl-prolyl isomerase that represses dendritic translation. Signals mediated by the excitatory neurotransmitter glutamate, which induces long-term potentiation (LTP) and memory formation, inhibit Pin1, enabling PKM{zeta} synthesis. PKM{zeta}, once translated, in turn inhibits Pin1, permitting persistent PKM{zeta} synthesis. In this way, PKM{zeta} may be up-regulated to the appropriate amounts for maintaining LTP and perpetuating our mental representations of the past.

* Corresponding author. E-mail, tsacktor{at}downstate.edu

Citation: T. C. Sacktor, PINing for Things Past. Sci. Signal. 3, pe9 (2010).

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