Autophosphorylation of αCaMKII is not a general requirement for NMDA receptor‐dependent LTP in the adult mouse
- 21 July 2006
- journal article
- Published by Wiley in The Journal of Physiology
- Vol. 574 (3), 805-818
- https://doi.org/10.1113/jphysiol.2006.111559
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.This publication has 53 references indexed in Scilit:
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