Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Carrier Proteins / physiology
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Endocytosis / physiology
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Exocytosis / physiology
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In Vitro Techniques
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Long-Term Potentiation / physiology
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N-Ethylmaleimide-Sensitive Proteins
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Neuronal Plasticity / physiology*
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Rats
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Rats, Sprague-Dawley
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Receptors, AMPA / physiology*
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Synapses / physiology*
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Synaptic Transmission / physiology*
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Vesicular Transport Proteins*
Substances
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Carrier Proteins
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Receptors, AMPA
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Vesicular Transport Proteins
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N-Ethylmaleimide-Sensitive Proteins
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Nsf protein, rat
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glutamate receptor ionotropic, AMPA 2