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

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

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57 Scopus citations

Abstract

Autophosphorylation of α-Ca2+/calmodulin kinase II (αCaMKII) 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 αCaMKII 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 αCaMKII signalling. Thus, the autophosphorylation of αCaMKII is not a general requirement for NMDA receptor-dependent LTP in the adult mouse.

Original languageEnglish (US)
Pages (from-to)805-818
Number of pages14
JournalJournal of Physiology
Volume574
Issue number3
DOIs
StatePublished - Aug 1 2006

ASJC Scopus subject areas

  • Physiology

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    Cooke, S. F., Wu, J., Plattner, F., Errington, M., Rowan, M., Peters, M., Hirano, A., Bradshaw, K. D., Anwyl, R., Bliss, T. V. P., & Giese, K. P. (2006). Autophosphorylation of αCaMKII is not a general requirement for NMDA receptor-dependent LTP in the adult mouse. Journal of Physiology, 574(3), 805-818. https://doi.org/10.1113/jphysiol.2006.111559