| First Author | Silva AJ | Year | 1992 |
| Journal | Science | Volume | 257 |
| Issue | 5067 | Pages | 201-6 |
| PubMed ID | 1378648 | Mgi Jnum | J:1421 |
| Mgi Id | MGI:49948 | Doi | 10.1126/science.1378648 |
| Citation | Silva AJ, et al. (1992) Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice [see comments]. Science 257(5067):201-6 |
| abstractText | 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. |
