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 α-calcium-calmodulin-dependent kinase II (α-CaMKII). The α-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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Dates
Type | When |
---|---|
Created | 18 years, 10 months ago (Oct. 5, 2006, 3:03 p.m.) |
Deposited | 1 year, 7 months ago (Jan. 10, 2024, 4:53 p.m.) |
Indexed | 3 days, 21 hours ago (Aug. 24, 2025, 6:52 p.m.) |
Issued | 33 years, 1 month ago (July 10, 1992) |
Published | 33 years, 1 month ago (July 10, 1992) |
Published Print | 33 years, 1 month ago (July 10, 1992) |
@article{Silva_1992, title={Deficient Hippocampal Long-Term Potentiation in α-Calcium-Calmodulin Kinase II Mutant Mice}, volume={257}, ISSN={1095-9203}, url={http://dx.doi.org/10.1126/science.1378648}, DOI={10.1126/science.1378648}, number={5067}, journal={Science}, publisher={American Association for the Advancement of Science (AAAS)}, author={Silva, Alcino J. and Stevens, Charles F. and Tonegawa, Susumu and Wang, Yanyan}, year={1992}, month=jul, pages={201–206} }