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Title: Acidosis, Acid-Sensing Ion Channels, and Neuronal Cell Death
Author: Wang, Yi-Zhi ; Xu, Tian-Le(徐天乐)
Source: MOLECULAR NEUROBIOLOGY
Issued Date: 2011
Volume: 44, Issue:3, Pages:350-358
Keyword: Acidosis ; ASIC1a ; Neuronal cell death ; Spermine ; Ischemic stroke ; EXTRACELLULAR ACIDOSIS ; H-1-NMR SPECTROSCOPY ; HUNTINGTONS-DISEASE ; SYNAPTIC-TRANSMISSION ; SPREADING DEPRESSION ; HIPPOCAMPAL-NEURONS ; PARKINSONS-DISEASE ; ALZHEIMERS-DISEASE ; ENDOTHELIAL-CELLS ; GABA(A) RECEPTORS
Subject: Neurosciences & Neurology
Corresponding Author: Xu, TL (reprint author), Shanghai Jiao Tong Univ, Sch Med, Div Neurosci, Dept Biochem & Mol Cell Biol,Inst Med Sci, 280 S Chongqing Rd, Shanghai 200025, Peoples R China,xu-happiness@shsmu.edu.cn
English Abstract: Acidosis is a common feature of many neuronal diseases and often accompanied with adverse consequences such as pain and neuronal injury. Before the discovery of acid-sensing ion channels (ASICs), protons were usually considered as a modulator of other ion channels, such as voltage-gated calcium channels, N-methyl-d-aspartate, and gamma-amino butyric acid(A) receptor channels. Accordingly, the functional effects of acidosis were considered as consequences of modulations of these channels. Since the first cloning of ASICs in 1997, the conventional view on acidosis-mediated pain and cell injury has been dramatically changed. To date, ASICs, which are directly activated by extracellular protons, are shown to mediate most of the acidosis-associated physiological and pathological functions. For example, ASIC1a channels are reported to mediate acidosis-induced ischemic neuronal death. In this article, we will review the possible mechanisms that underlie ASIC1a channel-mediated neuronal death and discuss ASIC1a channel modulators involved in this process.
Indexed Type: SCI
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/1520
Appears in Collections:神经所(总)_期刊论文

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Wang, Yi-Zhi; Xu, Tian-Le.Acidosis, Acid-Sensing Ion Channels, and Neuronal Cell Death,MOLECULAR NEUROBIOLOGY,2011,44(3):350-358
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