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This Article Full Text Full Text (PDF) Supplemental data All Versions of this Article: 583/2/537    most recent jphysiol.2007.136788v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sun, L. Articles by June Liu, S. Search for Related Content PubMed PubMed Citation Articles by Sun, L. Articles by June Liu, S. Related Collections Neuroscience

¹ Department of Biology, Penn State University, State College, PA 16802, USA

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.

(Received 17 May 2007; accepted after revision 15 June 2007; first published online 21 June 2007)
Corresponding author S. J. Liu: Department of Biology, 208 Mueller lab, Penn State University, State College, PA 16802, USA. Email: sjl16{at}psu.edu

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