Your browser version may not work well with NCBI's Web applications. More information here...
1: Science. 1992 Jul 10;257(5067):201-6.Click here to read Links
Comment in:
Science. 1992 Jul 10;257(5067):162-3.
Science. 1993 Oct 29;262(5134):760-3.

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

Silva AJ, Stevens CF, Tonegawa S, Wang Y.

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

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]