We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Enhanced long-term potentiation and impaired learning in mice with mutant postsynaptic density-95 protein.
- Authors
Migaud, M; Charlesworth, P; Dempster, M; Webster, L C; Watabe, A M; Makhinson, M; He, Y; Ramsay, M F; Morris, R G; Morrison, J H; O'Dell, T J; Grant, S G
- 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.
- Publication
Nature, 1998, Vol 396, Issue 6710, p433
- ISSN
0028-0836
- Publication type
Journal Article
- DOI
10.1038/24790