Role of AMPA receptor cycling in synaptic transmission and plasticity
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作者:
Lüscher, C
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机构:Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA
Lüscher, C
Xia, HH
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机构:Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA
Xia, HH
Beattie, EC
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机构:Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA
Beattie, EC
Carroll, RC
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机构:Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA
Carroll, RC
von Zastrow, M
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机构:Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA
von Zastrow, M
Malenka, RC
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机构:Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA
Malenka, RC
Nicoll, RA
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Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USAUniv Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA
Nicoll, RA
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机构:
[1] Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA
Compounds known to disrupt exocytosis or endocytosis were introduced into CA1 pyramidal cells while monitoring excitatory postsynaptic currents (EPSCs). Disrupting exocytosis or the interaction of GluR2 with NSF caused a gradual reduction in the AMPAR EPSC, while inhibition of endocytosis caused a gradual increase in the AMPAR EPSC. These manipulations had no effect on the NMDAR EPSC but prevented the subsequent induction of LTD. These results suggest that AMPARs, but not NMDARs, cycle into and out of the synaptic membrane at a rapid rate and that certain forms of synaptic plasticity may utilize this dynamic process.