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


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.

Pubmed ID: 1378648


  • Silva AJ
  • Stevens CF
  • Tonegawa S
  • Wang Y


Science (New York, N.Y.)

Publication Data

July 10, 1992

Associated Grants

  • Agency: NINDS NIH HHS, Id: 5 R01 NS 12961-17

Mesh Terms

  • Animals
  • Behavior, Animal
  • Blotting, Northern
  • Blotting, Southern
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Chromosome Mapping
  • DNA
  • Electrophysiology
  • Female
  • Hippocampus
  • Learning
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Mutant Strains
  • Mutagenesis, Site-Directed
  • Plasmids
  • Protein Kinases
  • RNA
  • Receptors, N-Methyl-D-Aspartate
  • Synapses
  • Transfection