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.
Pubmed ID: 1378648 RIS Download
Animals | Behavior, Animal | Blotting, Northern | Blotting, Southern | Calcium-Calmodulin-Dependent Protein Kinases | Chromosome Mapping | DNA | Electrophysiology | Female | Hippocampus | Learning | Male | Mice | Mice, Inbred BALB C | Mice, Mutant Strains | Mutagenesis, Site-Directed | Plasmids | Protein Kinases | RNA | Receptors, N-Methyl-D-Aspartate | Synapses | Transfection