期刊
NATURE NEUROSCIENCE
卷 21, 期 1, 页码 50-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41593-017-0030-z
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资金
- Canadian Institutes of Health Research (CIHR) [MOP119421, FDN154276]
- Canadian Natural Science and Engineering Research Council (NSERC) [RGPIN341498]
- Natural Science Foundation of China (NSFC) [31571040]
- NSFC and CIHR Joint Health Research Initiative Program [81161120543, CCI117959]
- Brain Canada
- Hospital for Sick Children Foundation
- Scientific Research Foundation of Graduate School of Southeast University, China
Long-term potentiation (LTP) and depression (LTD) at glutamatergic synapses are intensively investigated processes for understanding the synaptic basis for learning and memory, but the underlying molecular mechanisms remain poorly understood. We have made three mouse lines where the C-terminal domains (CTDs) of endogenous AMPA receptors (AMPARs), the principal mediators of fast excitatory synaptic transmission, are specifically exchanged. These mice display profound deficits in synaptic plasticity without any effects on basal synaptic transmission. Our study reveals that the CTDs of GluA1 and GluA2, the key subunits of AMPARs, are necessary and sufficient to drive NMDA receptor-dependent LTP and LTD, respectively. In addition, these domains exert differential effects on spatial and contextual learning and memory. These results establish dominant roles of AMPARs in governing bidirectional synaptic and behavioral plasticity in the CNS.
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