Literature DB >> 16728448

Autophosphorylation of alphaCaMKII is not a general requirement for NMDA receptor-dependent LTP in the adult mouse.

Sam F Cooke1, Jianqun Wu, Florian Plattner, Michael Errington, Michael Rowan, Marco Peters, Ayumi Hirano, Karl D Bradshaw, Roger Anwyl, Timothy V P Bliss, K Peter Giese.   

Abstract

Autophosphorylation of alpha-Ca2+/calmodulin kinase II (alphaCaMKII) at Thr286 is thought to be a general effector mechanism for sustaining transcription-independent long-term potentiation (LTP) at pathways where LTP is NMDA receptor-dependent. We have compared LTP at two such hippocampal pathways in mutant mice with a disabling point mutation at the Thr286 autophosphorylation site. We find that autophosphorylation of alphaCaMKII is essential for induction of LTP at Schaffer commissural-CA1 synapses in vivo, but is not required for LTP that can be sustained over days at medial perforant path-granule cell synapses in awake mice. At these latter synapses LTP is supported by cyclic AMP-dependent signalling in the absence of alphaCaMKII signalling. Thus, the autophosphorylation of alphaCaMKII is not a general requirement for NMDA receptor-dependent LTP in the adult mouse.

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Year:  2006        PMID： 16728448      PMCID： PMC1817742          DOI： 10.1113/jphysiol.2006.111559

Source DB:  PubMed          Journal:  J Physiol        ISSN： 0022-3751            Impact factor:   5.182


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