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Science 10 July 1992: Vol. 257. no. 5067, pp. 201 - 206 DOI: 10.1126/science.1378648
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Articles
Science, Vol 257, Issue 5067, 201-206
Copyright © 1992 by American Association for the Advancement of Science
Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice
AJ Silva,
CF Stevens,
S Tonegawa,
and
Y Wang
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.
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