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Autonomous CaMKII mediates both LTP and LTD using a mechanism for differential substrate site selection.

Abstract：

:Traditionally, hippocampal long-term potentiation (LTP) of synaptic strength requires Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) and other kinases, whereas long-term depression (LTD) requires phosphatases. Here, we found that LTD also requires CaMKII and its phospho-T286-induced "autonomous" (Ca(2+)-independent) activity. However, whereas LTP is known to induce phosphorylation of the AMPA-type glutamate receptor (AMPAR) subunit GluA1 at S831, LTD instead induced CaMKII-mediated phosphorylation at S567, a site known to reduce synaptic GluA1 localization. GluA1 S831 phosphorylation by "autonomous" CaMKII was further stimulated by Ca(2+)/CaM, as expected for traditional substrates. By contrast, GluA1 S567 represents a distinct substrate class that is unaffected by such stimulation. This differential regulation caused GluA1 S831 to be favored by LTP-type stimuli (strong but brief), whereas GluA1 S567 was favored by LTD-type stimuli (weak but prolonged). Thus, requirement of autonomous CaMKII in opposing forms of plasticity involves distinct substrate classes that are differentially regulated to enable stimulus-dependent substrate-site preference.

journal_name

Cell Rep

journal_title

Cell reports

authors

Coultrap SJ,Freund RK,O'Leary H,Sanderson JL,Roche KW,Dell'Acqua ML,Bayer KU

doi

10.1016/j.celrep.2014.01.005

subject

Has Abstract

pub_date

2014-02-13 00:00:00

pages

431-7

issue

3

issn

2211-1247

pii

S2211-1247(14)00006-0

journal_volume

6

pub_type

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