PKMζ Maintains Late Long-Term Potentiation byN-Ethylmaleimide-Sensitive Factor/GluR2-Dependent Trafficking of Postsynaptic AMPA Receptors

• DOI: 10.1523/jneurosci.0223-08.2008
• Publication Date: 2008-07-30T16:38:15Z
• Authors: Yudong Yao; Matthew Taylor Kelly; Sreedharan Sajikumar; Peter Serrano; Dezhi Tian; Peter John Bergold; Julietta Uta Frey; Todd Charlton Sac...
• Keywords: Postsynaptic density; Long-term depression

Although the maintenance mechanism of late long-term potentiation (LTP) is critical for storage memory, expression synaptic enhancement during late-LTP unknown. The autonomously active protein kinase C isoform, Mζ (PKMζ), a core molecule maintaining late-LTP. Here we show that PKMζ maintains through persistent N -ethylmaleimide-sensitive factor (NSF)/glutamate receptor subunit 2 (GluR2)-dependent trafficking AMPA receptors (AMPARs) to synapse. Intracellular perfusion into CA1 pyramidal cells causes postsynaptic AMPAR responses; this mediated NSF/GluR2 interactions but not vesicle-associated membrane protein-dependent exocytosis. may act NSF release GluR2-containing from reserve pool held at extrasynaptic sites by interacting with C-kinase 1 (PICK1), because disrupting GluR2/PICK1 mimic and occlude PKMζ-mediated potentiation. During LTP maintenance, directs trafficking, as measured NSF/GluR2-dependent increases GluR2/3-containing in synaptosomal fractions tetanized slices. Blocking reverses established synapses have undergone tagging capture. Thus, persistently modifying favor insertion sites.