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

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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.

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Authors and Affiliations

  1. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia

    I. V. Smolensky & A. V. Zaitsev

  2. Department of Experimental Neurology, National Institute of Mental Health, Prague, Czech Republic

    S. V. Ovsepian

  3. Department of Psychiatry and Medical Psychology, Third Faculty of Medicine, Charles University, Prague, Czech Republic

    S. V. Ovsepian

  4. International Centre for Neurotherapeutics, Dublin City University, Dublin, Ireland

    S. V. Ovsepian

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  1. I. V. Smolensky
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  2. S. V. Ovsepian
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  3. A. V. Zaitsev
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Correspondence to A. V. Zaitsev.

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Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 105, No. 9, pp. 1096–1112, September, 2019.

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Smolensky, I.V., Ovsepian, S.V. & Zaitsev, A.V. Glutamate Transporters (EAAT-1–3) as a Factor in the Pathogenesis and a Potential Therapeutic Target in Epilepsy. Neurosci Behav Physi 50, 777–786 (2020). https://doi.org/10.1007/s11055-020-00965-4

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  • DOI: https://doi.org/10.1007/s11055-020-00965-4

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