Negative modulation of NMDA receptor channel function by DREAM/calsenilin/KChIP3 provides neuroprotection?

Negative modulation of NMDA receptor channel function by DREAM/calsenilin/KChIP3 provides neuroprotection?
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DREAM/calsenilin/KChIP3 对 NMDA 受体通道功能的负调节可提供神经保护吗?

DOI:
10.3389/fnmol.2012.00039
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发表时间:
2012
影响因子:
4.8
通讯作者:
Wang Y
Wang Y
中科院分区:
医学2区
文献类型:
--
作者:
Wang K;Wang Y

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N-甲基-D-天冬氨酸受体(NMDAR)是谷氨酸门控离子通道,对钙离子高度渗透,对兴奋性神经传递至关重要。NMDARs因其在突触可塑性和兴奋性毒性中的作用而受到广泛关注。最近积累的证据表明,NMDAR是负调控的细胞内钙结合蛋白。NMDAR功能的钙依赖性抑制作为一种反馈机制,能够调节随后的Ca 2+进入突触后细胞,并可能提供治疗NMDAR介导的兴奋性毒性损伤的替代方法。本文综述了DREAM/calsenilin/KChIP 3对NMDAR功能负调控的研究进展。
N-methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion channels highly permeable to calcium and essential to excitatory neurotransmission. The NMDARs have attracted much attention because of their role in synaptic plasticity and excitotoxicity. Evidence has recently accumulated that NMDARs are negatively regulated by intracellular calcium binding proteins. The calcium-dependent suppression of NMDAR function serves as a feedback mechanism capable of regulating subsequent Ca2+ entry into the postsynaptic cell, and may offer an alternative approach to treating NMDAR-mediated excitotoxic injury. This short review summarizes the recent progress made in understanding the negative modulation of NMDAR function by DREAM/calsenilin/KChIP3, a neuronal calcium sensor (NCS) protein.
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