Glycolysis in energy metabolism during seizures |
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| Authors: | Heng Yang Jiongxing Wu Ren Guo Yufen Peng Wen Zheng Ding Liu Zhi Song |
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| Affiliation: | Heng Yang (Department of Neurology, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China)； Jiongxing Wu (Department of Neurology, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China)； Ren Guo (Department of Pharmacy, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China)； Yufen Peng (Department of Neurology, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China)； Wen Zheng (Department of Neurology, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China)； Ding Liu (Department of Neurology, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China)； Zhi Song (Department of Neurology, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan Province, China)； |
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| 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-minobutyric acid, and changes in the intra- and extracellular environment. |
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| Keywords: | neural regeneration reviews epilepsy energy metabolism glycolysis epileptogenesis termination ATP aerobic metabolism 6-diphosphate kinase-1 N-methyl-D-aspartate receptor acid-sensitive 1A ion channel γ-aminobutyric acid intra- and extracellular environment voltage-gated Na+ and Ca2+ adenosine receptors ATP receptor grants-supported paper neuroregeneration |
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