期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 583, 期 2, 页码 537-553出版社
WILEY
DOI: 10.1113/jphysiol.2007.136788
关键词
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资金
- Direct For Biological Sciences
- Division Of Integrative Organismal Sys [0964517] Funding Source: National Science Foundation
- NINDS NIH HHS [R01 NS058867] Funding Source: Medline
The repetitive activation of synaptic glutamate receptors can induce a lasting change in the number or subunit composition of synaptic AMPA receptors (AMPARs). However, NMDA receptors that are present extrasynaptically can also be activated by a burst of presynaptic activity, and thus may be involved in the induction of synaptic plasticity. Here we show that the physiological-like activation of extrasynaptic NMDARs induces a lasting change in the synaptic current, by changing the subunit composition of AMPARs at the parallel fibre-to-cerebellar stellate cell synapse. This extrasynaptic NMDAR-induced switch in synaptic AMPARs from GluR2-lacking (Ca2+-permeable) to GluR2-containing (Ca2+-impermeable) receptors requires the activation of protein kinase C (PKC). These results indicate that the activation of extrasynaptic NMDARs; by glutamate spillover is an important mechanism that detects the pattern of afferent activity and subsequently exerts a remote regulation of AMPAR subtypes at the synapse via a PKC-dependent pathway.
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