Autophosphorylation at Thr 286 of the α Calcium-Calmodulin Kinase II in LTP and Learning

• DOI: 10.1126/science.279.5352.870
• Publication Date: 2002-07-27T09:49:42Z
• Authors: Karl Peter Giese; Nikolai B. Fedorov; Robert K. Filipko...; Alcino J. Silva
• Keywords: 6-Cyano-7-nitroquinoxaline-2,3-dione; 0303 health sciences; Patch-Clamp Techniques; Pyramidal Cells; Long-Term Potentiation; Hippocampus; Receptors, N-Methyl-D-Aspartate; Mice, Mutant Strains; Mice, Inbred C57BL; Mice; 03 medical and health sciences; Phosphothreonine; 2-Amino-5-phosphonovalerate; Calmodulin; Calcium-Calmodulin-Dependent Protein Kinases; Gene Targeting; Animals; Picrotoxin; Point Mutation; Phosphorylation; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Maze Learning

The calcium-calmodulin–dependent kinase II (CaMKII) is required for hippocampal long-term potentiation (LTP) and spatial learning. In addition to its calcium-calmodulin (CaM)–dependent activity, CaMKII can undergo autophosphorylation, resulting in CaM-independent activity. A point mutation was introduced into the αCaMKII gene that blocked autophosphorylation of threonine at position 286 (Thr ) this without affecting CaM-dependent mutant mice had no N -methyl- d -aspartate receptor–dependent LTP CA1 area showed learning Morris water maze. Thus, Thr appears be