Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice.
As a first step in a program to use genetically altered mice in the study of memory mechanisms, mutant mice were produced that do not express the alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII). The alpha-CaMKII is highly enriched in postsynaptic densities of hippocampus and neocortex and may be involved in the regulation of long-term potentiation (LTP). Such mutant mice exhibited mostly normal behaviors and presented no obvious neuroanatomical defects. Whole cell recordings reveal that postsynaptic mechanisms, including N-methyl-D-aspartate (NMDA) receptor function, are intact. Despite normal postsynaptic mechanisms, these mice are deficient in their ability to produce LTP and are therefore a suitable model for studying the relation between LTP and learning processes.
Silva
A J
AJ
Howard Hughes Medical Institute, Center for Cancer Research, Cambridge, MA.
Stevens
C F
CF
Tonegawa
S
S
Wang
Y
Y
D000818:Animals; D001522:Behavior, Animal / Q000502:physiology; D015152:Blotting, Northern; D015139:Blotting, Southern; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D002874:Chromosome Mapping; D004247:DNA / Q000032:analysis; D004594:Electrophysiology; D005260:Female; D006624:Hippocampus / Q000502:physiology*; D007858:Learning / Q000502:physiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008817:Mice, Mutant Strains / Q000235:genetics*; D016297:Mutagenesis, Site-Directed; D010957:Plasmids; D011494:Protein Kinases / Q000172:deficiency* / Q000502:physiology*; D012313:RNA / Q000032:analysis; D016194:Receptors, N-Methyl-D-Aspartate; D013569:Synapses / Q000502:physiology; D014162:Transfection
D016194:Receptors, N-Methyl-D-Aspartate; D012313:RNA; D004247:DNA; D011494:Protein Kinases; D017871:Calcium-Calmodulin-Dependent Protein Kinases