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

Nature | Dec 3, 1998

http://www.ncbi.nlm.nih.gov/pubmed/9853749

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 RIS Download

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

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Associated grants

  • Agency: Wellcome Trust, Id:

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