Glutamate Transporters (EAAT-1–3) as a Factor in the Pathogenesis and a Potential Therapeutic Target in Epilepsy

被引：0
作者：
Smolensky I.V. [1 ]
Ovsepian S.V. [2 ,3 ,4 ]
Zaitsev A.V. [1 ]
机构：
[1] Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg
[2] Department of Experimental Neurology, National Institute of Mental Health, Prague
[3] Department of Psychiatry and Medical Psychology, Third Faculty of Medicine, Charles University, Prague
[4] International Centre for Neurotherapeutics, Dublin City University, Dublin
来源：
Neuroscience and Behavioral Physiology | 2020年 / 50卷 / 6期
关键词：
ceftriaxone; epilepsy; excitatory amino acid transporter; glutamate; model of epilepsy;
D O I：
10.1007/s11055-020-00965-4
中图分类号：
学科分类号：
摘要：
Epilepsy is one of the commonest neurological diseases, though convulsive seizures cannot be completely cured in 30% of patients, such that there is a need to develop new pharmacological approaches to its treatment. In some pathological states, including drug-resistant forms of epilepsy, the mechanisms removing glutamate from the synaptic cleft may be impaired, so one potential approach to these pathological states may be associated with actions on glutamate transporters. The present review analyzes contemporary data on changes in the expression of excitatory amino acid transporter proteins (EAAT) in human epilepsy and in animal models of convulsive states and epilepsy. Mechanisms of actions on the expression and activity of transporters as potential therapeutic targets for the treatment of convulsive states are considered, special attention being paid to analysis of the use of the antibiotic ceftriaxone, which increases the expression and activity of EAAT-2. © 2020, Springer Science+Business Media, LLC, part of Springer Nature.
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页码：777 / 786
页数：9
相关论文
共 123 条
[1]  
Meyer A.C., Dua T., Ma J., Et al., Global disparities in the epilepsy treatment gap: a systematic review, Bull. World Health Organ., 88, 4, pp. 260-266, (2010)
[2]  
Moshe S.L., Perucca E., Ryvlin P., Tomson T., Epilepsy: New advances, Lancet, 385, 9971, pp. 884-898, (2015)
[3]  
Loscher W., Klitgaard H., Twyman R.E., Schmidt D., New avenues for anti-epileptic drug discovery and development, Nat. Rev. Drug Discov., 12, 10, pp. 757-776, (2013)
[4]  
Barker-Haliski M., White H.S., Glutamatergic Mechanisms Associated with Seizures and Epilepsy, Cold Spring Harb. Perspect. Med., 5, 8, (2015)
[5]  
Traynelis S.F., Wollmuth L.P., McBain C.J., Et al., Glutamate receptor ion channels: Structure, regulation, and function, Pharmacol. Rev., 62, 3, pp. 405-496, (2010)
[6]  
Albrecht J., Zielinska M., Mechanisms of excessive extracellular glutamate accumulation in temporal lobe epilepsy, Neurochem. Res., 42, 6, pp. 1724-1734, (2017)
[7]  
Eid T., Gruenbaum S.E., Dhaher R., Et al., The glutamate-glutamine cycle in epilepsy, Adv. Neurobiol., 13, pp. 351-400, (2016)
[8]  
Bouvier M., Szatkowski M., Amato A., Attwell D., The glial cell glutamate uptake carrier countertransports pH-changing anions, Nature, 360, 6403, pp. 471-474, (1992)
[9]  
Benveniste H., Drejer J., Schousboe A., Diemer N.H., Elevation of the extracellular concentrations of glutamate and aspartate in rat hippocampus during transient cerebral ischemia monitored by intracerebral microdialysis, J. Neurochem., 43, 5, pp. 1369-1374, (1984)
[10]  
Lehmann A., Isacsson H., Hamberger A., Effects of in vivo administration of kainic acid on the extracellular amino acid pool in the rabbit hippocampus, J. Neurochem., 40, 5, pp. 1314-1320, (1983)
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