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


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1998-12

AUTHORS

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, Seth G. N. Grant

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. More... »

PAGES

433-439

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/24790

DOI

http://dx.doi.org/10.1038/24790

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1047999009

PUBMED

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


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