Actin polymerization regulates the synthesis of PKMζ in LTP

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 synt...

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Bibliographic Details
Published in:Neuropharmacology 2007, Vol.52 (1), p.41-45
Main Authors: Kelly, Matthew Taylor, Yao, Yudong, Sondhi, Rachna, Sacktor, Todd Charlton
Format: Article
Language:English
Subjects:
aPKC
Atypical PKC
Cytoskeleton
LTP
PKM zeta
PKMzeta
Structure
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Summary: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 (PKMζ). Here we show that preventing actin polymerization during LTP with latrunculin B blocks de novo protein synthesis of PKMζ. In contrast, the agent has minimal effects on the potentiation of AMPA receptors mediated by postsynaptically perfused PKMζ or on LTP expression. Thus actin filaments formed by tetanization enhance the efficiency of the synthesis of PKMζ that maintains LTP.
ISSN:0028-3908
1873-7064
DOI:10.1016/j.neuropharm.2006.07.002