Dynamin-dependent endocytosis of ionotropic glutamate receptors

Proceedings of the National Academy of Sciences of the United States of America - Tập 96 Số 24 - Trang 14112-14117 - 1999
Reed C. Carroll1, Eric C. Beattie1, Houhui Xia1, Christian Lüscher1, Yoram Altschuler1, Roger A. Nicoll1, Robert C. Malenka1, Mark von Zastrow1
1Departments of Psychiatry, Cellular and Molecular Pharmacology, Anatomy, and Physiology, University of California, San Francisco, CA 94143

Tóm tắt

Little is known about the mechanisms that regulate the number of ionotropic glutamate receptors present at excitatory synapses. Herein, we show that GluR1-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (AMPARs) are removed from the postsynaptic plasma membrane of cultured hippocampal neurons by rapid, ligand-induced endocytosis. Although endocytosis of AMPARs can be induced by high concentrations of AMPA without concomitant activation of N -methyl- d -aspartate (NMDA) receptors (NMDARs), NMDAR activation is required for detectable endocytosis induced by synaptically released glutamate. Activated AMPARs colocalize with AP2, a marker of endocytic coated pits, and endocytosis of AMPARs is blocked by biochemical inhibition of clathrin-coated pit function or overexpression of a dominant-negative mutant form of dynamin. These results establish that ionotropic receptors are regulated by dynamin-dependent endocytosis and suggest an important role of endocytic membrane trafficking in the postsynaptic modulation of neurotransmission.

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10.1146/annurev.ne.17.030194.000335

10.1016/S0959-4388(98)80062-7

10.1016/0166-2236(93)90093-2

10.1016/S0896-6273(00)80662-5

10.1016/S0896-6273(00)80362-1

10.1016/S0896-6273(00)80565-6

10.1038/4532

10.1038/10172

10.1073/pnas.95.12.7097

10.1016/S0896-6273(00)80962-9

10.1126/science.284.5421.1811

10.1038/8123

10.1523/JNEUROSCI.19-04-01263.1999

10.1016/S0092-8674(00)80578-4

10.1046/j.1471-4159.1995.65031146.x

10.1083/jcb.108.2.389

10.1083/jcb.143.7.1871

10.1016/S0021-9258(17)32329-3

10.1016/0955-0674(95)80013-1

10.1146/annurev.physiol.60.1.347

10.1523/JNEUROSCI.15-06-04328.1995

10.1242/jcs.87.2.203

10.1146/annurev.cb.06.110190.001055

10.1096/fasebj.9.14.7589986

10.1016/0006-2952(84)90447-7

10.1016/S0896-6273(00)80146-4

10.1083/jcb.127.4.915

10.1083/jcb.122.3.565

10.1083/jcb.122.3.553

10.1016/0092-8674(94)90517-7

10.1016/S0959-4388(97)80059-1

10.1016/0012-1606(90)90212-2

10.1038/351411a0

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Proceedings of the National Academy of Sciences of the United States of America

Tập 96 Số 24

14112-14117

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