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

Martine Migaud, Paul Charlesworth, Maureen Dempster, Lorna C. Webster, Ayako M. Watabe, Michael Makhinson, Yong He, Mark F. Ramsay, Richard G. M. Morris, John H. Morrison, Thomas J. O'Dell and Seth G. N. Grant ()
Additional contact information
Martine Migaud: Centre for Genome Research, and Centre for Neuroscience, University of Edinburgh
Paul Charlesworth: Centre for Genome Research, and Centre for Neuroscience, University of Edinburgh
Maureen Dempster: Centre for Genome Research, and Centre for Neuroscience, University of Edinburgh
Lorna C. Webster: Centre for Genome Research, and Centre for Neuroscience, University of Edinburgh
Ayako M. Watabe: School of Medicine, University of California at Los Angeles
Michael Makhinson: School of Medicine, University of California at Los Angeles
Yong He: Fishberg Research Centre for Neurobiology, Mount Sinai School of Medicine
Mark F. Ramsay: Centre for Neuroscience, University of Edinburgh
Richard G. M. Morris: Centre for Neuroscience, University of Edinburgh
John H. Morrison: Fishberg Research Centre for Neurobiology, Mount Sinai School of Medicine
Thomas J. O'Dell: School of Medicine, University of California at Los Angeles
Seth G. N. Grant: Centre for Genome Research, and Centre for Neuroscience, University of Edinburgh

Nature, 1998, vol. 396, issue 6710, 433-439

Abstract: Abstract 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.

Date: 1998
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DOI: 10.1038/24790

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