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

55 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.

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ASJC Scopus subject areas

  • Physiology

Cite this

Cooke, S. F., Wu, J., Plattner, F., Errington, M., Rowan, M., Peters, M., ... 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