
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.
N-Methylaspartate, Neuronal Plasticity, Organophosphonates, Excitatory Postsynaptic Potentials, Glutamic Acid, Nuclear Proteins, Cell Cycle Proteins, Electric Stimulation, Peptide Fragments, Piperazines, Mice, Inbred C57BL, Benzodiazepines, Mice, Cerebellum, Animals, Calcium, Carrier Proteins, Excitatory Amino Acid Antagonists, Protein Kinase Inhibitors, Protein Kinase C
N-Methylaspartate, Neuronal Plasticity, Organophosphonates, Excitatory Postsynaptic Potentials, Glutamic Acid, Nuclear Proteins, Cell Cycle Proteins, Electric Stimulation, Peptide Fragments, Piperazines, Mice, Inbred C57BL, Benzodiazepines, Mice, Cerebellum, Animals, Calcium, Carrier Proteins, Excitatory Amino Acid Antagonists, Protein Kinase Inhibitors, Protein Kinase C
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