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Title: Coupling between NMDA receptor and acid-sensing ion channel contributes to ischemic neuronal death
Author: Gao, J ; Duan, B ; Wang, DG ; Deng, XH ; Zhang, GY ; Xu, L ; Xu, TL(徐天乐)
Source: NEURON
Issued Date: 2005
Volume: 48, Issue:4, Pages:635-646
Keyword: PROTEIN-KINASE-II ; SUBUNIT MESSENGER-RNAS ; D-ASPARTATE RECEPTOR ; CELL-DEATH ; FOREBRAIN ISCHEMIA ; GLUTAMATE NEUROTOXICITY ; HIPPOCAMPAL SYNAPSES ; GLUCOSE DEPRIVATION ; NERVOUS-SYSTEM ; NR2B SUBUNIT
Subject: Neurosciences & Neurology
Corresponding Author: Xu, TL (reprint author), Chinese Acad Sci, Inst Neurosci, Shanghai 200031, Peoples R China,tlxu@ion.ac.cn
English Abstract: Acid-sensing ion channels (ASICs) composed of ASIC1a subunit exhibit a high Ca2+ permeability and play important roles in synaptic plasticity and acid-induced cell death. Here, we show that ischemia enhances ASIC currents through the phosphorylation at Ser478 and Ser479 of ASIC1a, leading to exacerbated ischemic cell death. The phosphorylation is catalyzed by Ca2+/calmodulin-dependent protein kinase II (CaMKII) activity, as a result of activation of NR2B-containing N-methyl-D-aspartate subtype of glutamate receptors (NMDARs) during ischemia. Furthermore, NR2B-specific antagonist, CaMKII inhibitor, or overexpression of mutated form of ASIC1a with Ser478 or Ser479 replaced by alanine (ASICla-S478A, ASIC1a-S479A) in cultured hippocampal neurons prevented ischemia-induced enhancement of ASIC currents, cytoplasmic Ca2+ elevation, as well as neuronal death. Thus, NMDAR-CaMKII cascade is functionally coupled to ASICs and contributes to acidotoxicity during ischemia. Specific blockade of NMDAR/CaMKII-ASIC coupling may reduce neuronal death after ischemia and other pathological conditions involving excessive glutamate release and acidosis.
Indexed Type: SCI
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/1866
Appears in Collections:神经所(总)_期刊论文

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Gao, J; Duan, B; Wang, DG; Deng, XH; Zhang, GY; Xu, L; Xu, TL.Coupling between NMDA receptor and acid-sensing ion channel contributes to ischemic neuronal death,NEURON,2005,48(4):635-646
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