Postsynaptic membrane fusion and long-term potentiation
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作者:
Lledo, PM
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机构:Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA 94143 USA
Lledo, PM
Zhang, XY
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机构:Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA 94143 USA
Zhang, XY
Südhof, TC
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机构:Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA 94143 USA
Südhof, TC
Malenka, RC
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机构:Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA 94143 USA
Malenka, RC
Nicoll, RA
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Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA 94143 USAUniv Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA 94143 USA
Nicoll, RA
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机构:
[1] Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA
[3] Univ Texas, SW Med Ctr, Dept Mol Genet, Dallas, TX 75235 USA
[4] Univ Texas, SW Med Ctr, Howard Hughes Med Inst, Dallas, TX 75235 USA
[5] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA
The possibility that membrane fusion events in the postsynaptic cell may be required for the change in synaptic strength resulting from long-term potentiation (LTP) was examined. Introducing substances into the postsynaptic cell that block membrane fusion at a number of different steps reduced LTP. Introducing SNAP, a protein that promotes membrane fusion, into cells enhanced synaptic transmission, and this enhancement was significantly less when generated in synapses that expressed LTP. Thus, postsynaptic fusion events, which could be involved either in retrograde signaling or in regulating postsynaptic receptor function or both, contribute to LTP.