Changes in the Expression of Genes of the Glutamate Transporter and Subunits of the NMDA and AMPA Receptors in the Rat Amygdala in the Lithium–Pilocarpine Model of Epilepsy
- Authors: Zubareva O.E.1,2, Kovalenko A.A.1, Karyakin V.B.1, Kalemenev S.V.1, Lavrent’eva V.V.1, Magazanik L.G.1,3, Zaitsev A.V.1,4
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Affiliations:
- Sechenov Institute of Evolutionary Physiology and Biochemistry
- Aff4
- St. Petersburg State University
- Almazov National Medical Research Center
- Issue: Vol 12, No 3 (2018)
- Pages: 222-227
- Section: Experimental Articles
- URL: https://ogarev-online.ru/1819-7124/article/view/211528
- DOI: https://doi.org/10.1134/S1819712418030170
- ID: 211528
Cite item
Abstract
The molecular changes in the glutamatergic system of the rat amygdala were studied during the latent phase of the lithium–pilocarpine model of temporal lobe epilepsy in order to identify the potential involvement of these changes in epileptogenesis. The real-time PCR method was used to evaluate the mRNA expression of the NMDA and AMPA receptor subunits, as well as the excitatory amino acid transporter-2 (EAAT2) in the basolateral nucleus of the amygdala 7 days after the seizures caused by administration of pilocarpine. The results of the experiments were as follows: (1) an increase in the expression ratio of the GluN2a/GluN2b NMDA receptor subunits with an unchanged expression level of the GluN1 subunit; (2) increased expression of the GluA2 subunit of AMPA receptors with the invariance of GluA1, and (3) enhanced expression of the EAAT2. According to literature data, the expression of the same genes decreased in the hippocampus in the same model of epilepsy. Neurodegeneration was reported in both brain regions. The opposite changes in the expression of the glutamatergic system genes in the hippocampus and amygdala during the latent period of the lithium–pilocarpine model suggest the occurrence of factors that can both contribute to and hinder epileptogenesis.
About the authors
O. E. Zubareva
Sechenov Institute of Evolutionary Physiology and Biochemistry; Aff4
Author for correspondence.
Email: zubarevaoe@mail.ru
Russian Federation, St. Petersburg; prosp. Toreza, 44, St. Petersburg, 194223
A. A. Kovalenko
Sechenov Institute of Evolutionary Physiology and Biochemistry
Email: zubarevaoe@mail.ru
Russian Federation, St. Petersburg
V. B. Karyakin
Sechenov Institute of Evolutionary Physiology and Biochemistry
Email: zubarevaoe@mail.ru
Russian Federation, St. Petersburg
S. V. Kalemenev
Sechenov Institute of Evolutionary Physiology and Biochemistry
Email: zubarevaoe@mail.ru
Russian Federation, St. Petersburg
V. V. Lavrent’eva
Sechenov Institute of Evolutionary Physiology and Biochemistry
Email: zubarevaoe@mail.ru
Russian Federation, St. Petersburg
L. G. Magazanik
Sechenov Institute of Evolutionary Physiology and Biochemistry; St. Petersburg State University
Email: zubarevaoe@mail.ru
Russian Federation, St. Petersburg; St. Petersburg
A. V. Zaitsev
Sechenov Institute of Evolutionary Physiology and Biochemistry; Almazov National Medical Research Center
Email: zubarevaoe@mail.ru
Russian Federation, St. Petersburg; St. Petersburg
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