Autophosphorylation of alphaCaMKII is not a general requirement for NMDA receptor-dependent LTP in the adult mouse.
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.
Cooke
Sam F
SF
MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK. scooke@nimr.mrc.ac.uk
Wu
Jianqun
J
Plattner
Florian
F
Errington
Michael
M
Rowan
Michael
M
Peters
Marco
M
Hirano
Ayumi
A
Bradshaw
Karl D
KD
Anwyl
Roger
R
Bliss
Timothy V P
TV
Giese
K Peter
KP
D000200:Action Potentials / Q000502:physiology*; D019943:Amino Acid Substitution; D000818:Animals; D054737:Calcium-Calmodulin-Dependent Protein Kinase Kinase; D002478:Cells, Cultured; D006624:Hippocampus / Q000502:physiology*; D017774:Long-Term Potentiation / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D016297:Mutagenesis, Site-Directed; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*
D016194:Receptors, N-Methyl-D-Aspartate; D017346:Protein Serine-Threonine Kinases; D054737:Calcium-Calmodulin-Dependent Protein Kinase Kinase