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Science. 1992 Jul 10;257(5067):201-6.

Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice.

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  • 1Howard Hughes Medical Institute, Center for Cancer Research, Cambridge, MA.

Abstract

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.

PMID:
1378648
[PubMed - indexed for MEDLINE]
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