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线粒体复合体功能抑制对神经元离子通道和神经递质释放的影响(英文)

The influence of mitochondrial complex inhibition on neuronal ion channel and neurotransmitter release
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摘要 线粒体复合体功能抑制在很多神经系统退行性疾病中都有报道,因此线粒体复合体功能抑制对神经元功能的影响和机制备受关注。神经元功能的完成离不开动作电位的产生和动作电位诱发的神经递质释放。神经元动作电位的产生主要是由电压依赖的钠离子通道和电压依赖的钾离子通道共同介导的。而电压依赖的钙通道直接参与了神经递质释放。某些病理原因导致的这些离子通道的功能异常会直接影响神经元功能,甚至导致神经元死亡。因此研究线粒体复合体抑制对神经元离子通道和神经递质释放的影响和机制对于了解相关神经系统疾病发病机制非常重要。本文对以上方面的研究进展做一综述。 Mitochondrial complex inhibition has been described in the pathophysiology of many neurodegenerative diseases, and the functional changes of neuron induced by mitochondrial complex inhibition and the mechanism are concerned. Neuronal function depends on action potentials and neurotransmitter release. Voltage dependent sodium/potassium ion channels mediate generation of neuron action potentials. And voltage dependent calcium ion channels are directly involved in the process of neurotransmitter release. The functional changes of those ion channels under some pathological conditions can induce neuron dysfunction, even death. Therefore, understanding the influence of mitochondrial complex inhibition on neuronal ion channels and neurotransmitter release is helpful to illuminate the pathophysiology of neurodegenerative diseases. This review will highlight recent progress in this field.
作者 来滨 郑平
出处 《生理学报》 CAS CSCD 北大核心 2012年第6期713-720,共8页 Acta Physiologica Sinica
基金 supported by the National Natural Science Foundation of China (No.30900424,30670653 and 30821002) the National Basic Research Development Program,Ministry of Science and Technology of China (No.2009CB522001)
关键词 线粒体复合体功能抑制 离子通道 神经递质释放 mitochondrial complex inhibition ion channels neurotransmitter release
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参考文献52

  • 1Lin MT, Beal MF. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature 2006; 443 (7113): 787-795.
  • 2Schapira AH. Human complex I defects in neurodegenerative diseases. Biochim Biophys Acta 1998; 1364: 216-270.
  • 3Moreira PI, Zhu X, Wang X, Lee HG, Nunomura A, Petersen RB, Perry G, Smith MA. Mitochondria: a therapeutic target in neurodegeneration. Biochim Biophys Acta 2010; 1802: 212-220.
  • 4Shuai JW, Jung P. Optimal ion channel clustering for intracellular calcium signaling. Proc Natl Acad Sci U S A 2003; 100(2): 506-510.
  • 5Cruz JS, Silva DF, Ribeiro LA, Araujo IG, Magalhaes N, Medeiros A, Freitas C, Araujo IC, Oliveira FA. Resurgent Na^+ current: a new avenue to neuronal excitability control. Life Sci 2011; 89(15-16): 564-569.
  • 6Taylor CP, Burke SP, Weber ML. Hippocampal slices: glutamate overflow and cellular damage from ischemia are reduced by sodium-channel blockade. J Neurosci Methods 1995; 59: 121-128.
  • 7Astrup J, Sorensen PM, Sorensen HR. Oxygen and glucose consumption related to Na^+-K^+ transport in canine brain. Stroke 1981; 12: 726-730.
  • 8Weber ML, Taylor CP. Damage from oxygen and glucose deprivation in hippocampal slices is prevented by tetrodotoxin, lidocaine and phenytoin without blockade of action potentials. Brain Res 1994; 664: 167-177.
  • 9Prenen GH, Go KG, Postema F, Zuiderveen F, Korf J. Cerebral cation shifts in hypoxic-ischemic brain damage are prevented by the sodium channel blocker tetrodotoxin. Exp Neurol 1988; 99: 118-132.
  • 10Hammarstrom AK, Gage PW. Inhibition of oxidative metabolism increases persistent sodiumcurrent in rat CA1 hippocampal neurons. J Physiol 1998; 510(3): 735-741.

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