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• W1965632015 abstract "Protein kinase Mζ (PKMζ), a constitutively active, atypical PKC isoform, enhances synaptic strength during the maintenance of long-term potentiation (LTP). Here we examine the mechanism by which PKMζ increases synaptic transmission. Postsynaptic perfusion of PKMζ during whole-cell recordings of CA1 pyramidal cells strongly potentiated the amplitude of AMPA receptor (AMPAR)-mediated miniature EPSCs (mEPSCs). Nonstationary fluctuation analysis of events recorded before and after PKMζ enhancement showed that the kinase doubled the number of functional postsynaptic AMPAR channels. After sustained potentiation, application of a PKMζ inhibitor reversed the increase in functional channel number to basal levels, suggesting that persistent increase of PKMζ is required to maintain the postsynaptic localization of a mobile subpopulation of receptors. The kinase did not affect other sites of LTP expression, including presynaptic transmitter release, silent synapse conversion, or AMPAR unit conductance. Thus PKMζ functions specifically to establish and maintain long-term increases in active postsynaptic AMPAR number. © 2006 Wiley-Liss, Inc." @default.
• W1965632015 created "2016-06-24" @default.
• W1965632015 creator A5045931689 @default.
• W1965632015 creator A5083331353 @default.
• W1965632015 creator A5086067249 @default.
• W1965632015 date "2006-01-01" @default.
• W1965632015 modified "2023-09-27" @default.
• W1965632015 title "Protein kinase Mζ enhances excitatory synaptic transmission by increasing the number of active postsynaptic AMPA receptors" @default.
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• W1965632015 doi "https://doi.org/10.1002/hipo.20171" @default.
• W1965632015 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16463388" @default.
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