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突触后α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体（AMPARs）的表面迁移率调节突触传递。

Surface mobility of postsynaptic AMPARs tunes synaptic transmission.

作者信息

Heine Martin, Groc Laurent, Frischknecht Renato, Béïque Jean-Claude, Lounis Brahim, Rumbaugh Gavin, Huganir Richard L, Cognet Laurent, Choquet Daniel

机构信息

CNRS, UMR 5091, Université Bordeaux, Bordeaux, France.

出版信息

Science. 2008 Apr 11;320(5873):201-5. doi: 10.1126/science.1152089.

DOI:10.1126/science.1152089
PMID:18403705
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2715948/
Abstract

AMPA glutamate receptors (AMPARs) mediate fast excitatory synaptic transmission. Upon fast consecutive synaptic stimulation, transmission can be depressed. Recuperation from fast synaptic depression has been attributed solely to recovery of transmitter release and/or AMPAR desensitization. We show that AMPAR lateral diffusion, observed in both intact hippocampi and cultured neurons, allows fast exchange of desensitized receptors with naïve functional ones within or near the postsynaptic density. Recovery from depression in the tens of millisecond time range can be explained in part by this fast receptor exchange. Preventing AMPAR surface movements through cross-linking, endogenous clustering, or calcium rise all slow recovery from depression. Physiological regulation of postsynaptic receptor mobility affects the fidelity of synaptic transmission by shaping the frequency dependence of synaptic responses.

摘要

α-氨基-3-羟基-5-甲基-4-异恶唑丙酸型谷氨酸受体（AMPARs）介导快速兴奋性突触传递。在快速连续的突触刺激下，传递会受到抑制。快速突触抑制的恢复一直被认为仅仅归因于递质释放的恢复和/或AMPAR脱敏。我们发现，在完整的海马体和培养的神经元中均观察到的AMPAR横向扩散，使得脱敏受体能够与突触后致密区或其附近的未致敏功能性受体快速交换。在几十毫秒时间范围内从抑制中恢复，部分可以用这种快速受体交换来解释。通过交联、内源性聚集或钙升高来阻止AMPAR在表面的移动，都会减缓从抑制中的恢复。突触后受体流动性的生理调节通过塑造突触反应的频率依赖性来影响突触传递的保真度。

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