Publication Date:
1992-07-10
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silva, A J -- Stevens, C F -- Tonegawa, S -- Wang, Y -- 5 R01 NS 12961-17/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1992 Jul 10;257(5067):201-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Center for Cancer Research, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1378648" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Behavior, Animal/physiology
;
Blotting, Northern
;
Blotting, Southern
;
Calcium-Calmodulin-Dependent Protein Kinases
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Chromosome Mapping
;
DNA/analysis
;
Electrophysiology
;
Female
;
Hippocampus/*physiology
;
Learning/physiology
;
Male
;
Mice
;
Mice, Inbred BALB C
;
Mice, Mutant Strains/*genetics
;
Mutagenesis, Site-Directed
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Plasmids
;
Protein Kinases/*deficiency/*physiology
;
RNA/analysis
;
Receptors, N-Methyl-D-Aspartate
;
Synapses/physiology
;
Transfection
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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