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Enhanced long-term potentiation and impaired learning in mice with mutant postsynaptic density-95 protein.

Specific patterns of neuronal firing induce changes in synaptic strength that may contribute to learning and memory. If the postsynaptic NMDA (N-methyl-D-aspartate) receptors are blocked, long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission and the learning of spatial information are prevented. The NMDA receptor can bind a protein known as postsynaptic density-95 (PSD-95), which may regulate the localization of and/or signalling by the receptor. In mutant mice lacking PSD-95, the frequency function of NMDA-dependent LTP and LTD is shifted to produce strikingly enhanced LTP at different frequencies of synaptic stimulation. In keeping with neural-network models that incorporate bidirectional learning rules, this frequency shift is accompanied by severely impaired spatial learning. Synaptic NMDA-receptor currents, subunit expression, localization and synaptic morphology are all unaffected in the mutant mice. PSD-95 thus appears to be important in coupling the NMDA receptor to pathways that control bidirectional synaptic plasticity and learning.

Pubmed ID: 9853749

Authors

  • Migaud M
  • Charlesworth P
  • Dempster M
  • Webster LC
  • Watabe AM
  • Makhinson M
  • He Y
  • Ramsay MF
  • Morris RG
  • Morrison JH
  • O'Dell TJ
  • Grant SG

Journal

Nature

Publication Data

December 3, 1998

Associated Grants

  • Agency: Wellcome Trust, Id:

Mesh Terms

  • Animals
  • Electrophysiology
  • Gene Targeting
  • Guanylate Kinase
  • Hippocampus
  • Intracellular Signaling Peptides and Proteins
  • Learning
  • Learning Disorders
  • Long-Term Potentiation
  • Maze Learning
  • Membrane Proteins
  • Memory
  • Mice
  • Mice, Inbred C57BL
  • Models, Neurological
  • Mutation
  • Nerve Tissue Proteins
  • Receptors, N-Methyl-D-Aspartate
  • Signal Transduction
  • Synapses