MHC Ⅰ类分子调节 NMDA 受体功能和 AMPA 受体转运。
MHC class I modulates NMDA receptor function and AMPA receptor trafficking.
机构信息
Division of Biological Sciences, Section of Neurobiology, University of California at San Diego, La Jolla, CA 92093-0366, USA.
出版信息
Proc Natl Acad Sci U S A. 2010 Dec 21;107(51):22278-83. doi: 10.1073/pnas.0914064107. Epub 2010 Dec 6.
Abstract
Proteins of the major histocompatibility complex class I (MHCI) are known for their role in immunity and have recently been implicated in long-term plasticity of excitatory synaptic transmission. However, the mechanisms by which MHCI influences synaptic plasticity remain unknown. Here we show that endogenous MHCI regulates synaptic responses mediated by NMDA-type glutamate receptors (NMDARs) in the mammalian central nervous system (CNS). The AMPA/NMDA ratio is decreased at MHCI-deficient hippocampal synapses, reflecting an increase in NMDAR-mediated currents. This enhanced NMDAR response is not associated with changes in the levels, subunit composition, or gross subcellular distribution of NMDARs. Increased NMDAR-mediated currents in MHCI-deficient neurons are associated with characteristic changes in AMPA receptor trafficking in response to NMDAR activation. Thus, endogenous MHCI tonically inhibits NMDAR function and controls downstream NMDAR-induced AMPA receptor trafficking during the expression of plasticity.
摘要
主要组织相容性复合体 I 类（MHC I）蛋白以其在免疫中的作用而闻名，最近其在兴奋性突触传递的长期可塑性中也有涉及。然而，MHC I 影响突触可塑性的机制尚不清楚。本文中，我们发现内源性 MHC I 调节哺乳动物中枢神经系统（CNS）中 NMDA 型谷氨酸受体（NMDAR）介导的突触反应。在 MHC I 缺失的海马突触中，AMPA/NMDA 比值降低，反映出 NMDAR 介导的电流增加。这种增强的 NMDAR 反应与 NMDAR 水平、亚基组成或大体亚细胞分布没有变化有关。MHC I 缺失神经元中 NMDAR 介导的电流增加与 NMDAR 激活时 AMPA 受体转运的特征变化有关。因此，内源性 MHC I 紧张性地抑制 NMDAR 功能，并在可塑性表达过程中控制下游 NMDAR 诱导的 AMPA 受体转运。
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