Format

Send to

Choose Destination
See comment in PubMed Commons below
Neuropharmacology. 2007 Jan;52(1):41-5. Epub 2006 Aug 17.

Actin polymerization regulates the synthesis of PKMzeta in LTP.

Author information

1
Department of Physiology, The Robert F. Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, 450 Clarkson Ave., Brooklyn, NY 11203, USA.

Abstract

Changes in the actin-based synaptic cytoskeleton are important for long-term potentiation (LTP), but the mechanism linking actin filament formation and the persistence of enhanced synaptic transmission has not been described. Actin filaments form rapidly during LTP induction without new protein synthesis, but their effects on synaptic potentiation occur during protein synthesis-dependent late-LTP. Previous studies have shown that late-LTP is mediated by the synthesis of the persistently active, atypical PKC isoform, protein kinase Mzeta (PKMzeta). Here we show that preventing actin polymerization during LTP with latrunculin B blocks de novo protein synthesis of PKMzeta. In contrast, the agent has minimal effects on the potentiation of AMPA receptors mediated by postsynaptically perfused PKMzeta or on LTP expression. Thus actin filaments formed by tetanization enhance the efficiency of the synthesis of PKMzeta that maintains LTP.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center