中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (14): 1316-1326.doi: 10.3969/j.issn.1673-5374.2013.14.008

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

糖酵解在痫性发作中的能量代谢

  

  • 收稿日期:2012-12-04 修回日期:2013-03-27 出版日期:2013-05-15 发布日期:2013-05-15

Glycolysis in energy metabolism during seizures

Heng Yang1, Jiongxing Wu1, Ren Guo2, Yufen Peng1, Wen Zheng1, Ding Liu1, Zhi Song1   

  1. 1 Department of Neurology, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China
    2 Department of Pharmacy, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China
  • Received:2012-12-04 Revised:2013-03-27 Online:2013-05-15 Published:2013-05-15
  • Contact: Zhi Song, M.D., Professor, Department of Neurology, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China, johnnelyang@hotmail.com.
  • About author:Heng Yang☆, Studying for doctorate, Professor.

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摘要：

研究表明，痫性发作时可致糖酵解增加，而且糖酵解代谢产物乳酸可为痫性发作提供能量并参与痫性发作的终止。但在痫性发作中糖酵解的能量代谢特点是什么？糖酵解代谢产物乳酸如何参与癫痫供能？如何导致痫性发作的终止？鉴于此，作者综述了糖酵解参与痫性发作的可能作用机制。结果证实，在癫痫发作早期，糖酵解代谢产物乳酸参与痫性发作提供能量，随着癫痫发作的进展，乳酸降低了组织的pH值，导致人体出现代谢酸中毒，痫性发作终止。糖酵解代谢产物乳酸致酸中毒的具体机制为：乳酸可能抑制磷酸果糖激酶、N-甲基-D-天冬氨酸受体，激活酸敏感性1A型离子通道受体的功能表达，增强γ-氨基丁酸受体功能，改变细胞内外环境，以此抑制癫痫的发作。

关键词: 神经再生, 综述, 脑损伤, 癫痫, 能量代谢, 糖酵解, 致痫, ATP, 有氧代谢, 磷酸果糖激酶, N-甲基-D-天冬氨酸受体, 酸敏感性1A离子通道, γ-氨基丁酸, 细胞内外环境, 电压依赖性钠, 钙通道, 腺苷受体, ATP受体, 基金资助文章

Abstract:

Studies have shown that glycolysis increases during seizures, and that the glycolytic metabolite lactic acid can be used as an energy source. However, how lactic acid provides energy for seizures and how it can participate in the termination of seizures remains unclear. We reviewed possible mechanisms of glycolysis involved in seizure onset. Results showed that lactic acid was involved in seizure onset and provided energy at early stages. As seizures progress, lactic acid reduces the pH of tissue and induces metabolic acidosis, which terminates the seizure. The specific mechanism of lactic acid-induced acidosis involves several aspects, which include lactic acid-induced inhibition of the glycolytic enzyme 6-diphosphate kinase-1, inhibition of the N-methyl-D-aspartate receptor, activation of the acid-sensitive 1A ion channel, strengthening of the receptive mechanism of the inhibitory neurotransmitter γ-aminobutyric acid, and changes in the intra- and extracellular environment.