Glycolysis in energy metabolism during seizures  

Glycolysis in energy metabolism during seizures

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作  者:Heng Yang Jiongxing Wu Ren Guo Yufen Peng Wen Zheng Ding Liu Zhi Song 

机构地区:[1]Department of Neurology,Third Xiangya Hospital,Central South University [2]Department of Pharmacy,Third Xiangya Hospital,Central South University

出  处:《Neural Regeneration Research》2013年第14期1316-1326,共11页中国神经再生研究(英文版)

基  金:supported by the National Natural Science Foundation of China,No.30971534;125 Project of the Third Xiangya Hospital,China

摘  要: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 Y-aminobutyric acid, and changes in the intra- and extracellular environment.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 Y-aminobutyric acid, and changes in the intra- and extracellular environment.

关 键 词:neural regeneration reviews epilepsy energy metabolism GLYCOLYSIS EPILEPTOGENESIS terminationATP aerobic metabolism 6-diphosphate kinase-1 N-methyI-D-aspartate receptor acid-sensitive1A ion channel y-aminobutyric acid intra- and extracellular environment voltage-gated Na+ andCa2+ adenosine receptors ATP receptor grants-supported paper NEUROREGENERATION 

分 类 号:R742.1[医药卫生—神经病学与精神病学]

 

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