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This Article Full Text Full Text (PDF) Supplemental data All Versions of this Article: 574/3/805    most recent jphysiol.2006.111559v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cooke, S. F. Articles by Giese, K. P. Search for Related Content PubMed PubMed Citation Articles by Cooke, S. F. Articles by Giese, K. P. Related Collections Neuroscience

¹ MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK
² Department of Physiology, Trinity College Dublin, Dublin 2, Ireland
³ Wolfson Institute for Biomedical Research, University College London, London WC1E 1BT, UK

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

(Received 11 May 2006; accepted after revision 18 May 2006; first published online 25 May 2006)
Corresponding authors S. F. Cooke: National Institute for Medical Research, Mill Hill, London NW7 1AA, UK. Email: scooke{at}nimr.mrc.ac.uk; K. P. Giese: Wolfson Institute for Biomedical Research, University College London, London WC1E 1BT, UK. Email: p.giese{at}ucl.ac.uk

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