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Copper-dependent regulation of NMDA receptors by cellular prion protein: implications for neurodegenerative disorders

机译:细胞铜蛋白对NMDA受体的铜依赖性调节:对神经退行性疾病的影响

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摘要

AbstractN-Methyl-d-aspartate (NMDA) receptors mediate a wide range of important nervous system functions. Conversely, excessive NMDA receptor activity leads to cytotoxic calcium overload and neuronal damage in a wide variety of CNS disorders. It is well established that NMDA receptors are tightly regulated by a number of cell signalling pathways. Recently, it has been shown that NMDA receptor activity is modulated by cellular prion protein (PrPC) in a copper-dependent manner. Here we give an overview of the current state of knowledge concerning the novel concept of potent modulation of this receptor's kinetics by copper ions, and the interplay between NMDA receptors and PrPC in the context of neurological diseases such as Alzheimer's disease, epilepsy, pain and depression.
机译:摘要N-甲基-d-天冬氨酸(NMDA)受体介导广泛的重要神经系统功能。相反,过量的NMDA受体活性导致多种CNS疾病中的细胞毒性钙超载和神经元损伤。众所周知,NMDA受体受到许多细胞信号通路的严格调控。近年来,已经显示出NMDA受体活性被细胞蛋白(PrP C )以铜依赖性方式调节。在这里,我们概述了有关铜离子有效调节该受体动力学的新概念的当前知识状态,以及NMDA受体与PrP C 在神经系统疾病(如神经疾病)中的相互作用。阿尔茨海默氏病,癫痫,疼痛和抑郁症。

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