Mechanisms of Monoamine Oxidase Involvement in the Development of Hyperbaric Oxygen Seizures
- Authors: Zhilyaev S.Y.1, Basova I.N.1, Platonova T.F.1, Alekseeva O.S.1, Gavrisheva N.A.2, Demchenko I.T.1
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Affiliations:
- Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences
- Pavlov First Saint Petersburg State Medical University
- Issue: Vol 60, No 5 (2024)
- Pages: 526-534
- Section: EXPERIMENTAL ARTICLES
- URL: https://cijournal.ru/0044-4529/article/view/648109
- DOI: https://doi.org/10.31857/S0044452924050069
- EDN: https://elibrary.ru/XPEPWU
- ID: 648109
Cite item
Abstract
Hyperbaric oxygen (HBO2) breathing induces generalized tonic and clonic seizures through poorly understood mechanisms. The purpose of the research was to evaluate the mechanisms of involvement of monoamine oxidase (MAO) in the development of hyperbaric oxygen convulsions. In rats placed in a pressure chamber under an oxygen pressure of 5 ATA, convulsive reactions were analyzed after the administration of pyrazidol, a MAO-A inhibitor, and pargyline, a MAO-B inhibitor. Studies have shown a decrease in the activity of MAO isoforms in HBO2 as well as a delay in the development of seizures in animals with inhibition of MAO-A and MAO-B. The level of GABA in the brain decreased with HBO2, and inhibition of MAO-B with pargyline prevented the decrease in the inhibitory transmitter. The results indicate that MAO isoforms play an important role in regulating epileptogenesis in extreme hyperoxia. Hyperbaric oxygen, inhibiting the catalytic activity of MAO by transforming its molecular structure, leads to disruption of the regulation of the exchange of monoamine neurotransmitters and a decrease in the level of GABA in the brain, which together leads to an imbalance of excitation/inhibition processes in the central nervous system, which is the basis for the development of oxygen epilepsy.
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About the authors
S. Yu. Zhilyaev
Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences
Email: osa72@inbox.ru
Russian Federation, Saint Petersburg
I. N. Basova
Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences
Email: osa72@inbox.ru
Russian Federation, Saint Petersburg
T. F. Platonova
Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences
Email: osa72@inbox.ru
Russian Federation, Saint Petersburg
O. S. Alekseeva
Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences
Author for correspondence.
Email: osa72@inbox.ru
Russian Federation, Saint Petersburg
N. A. Gavrisheva
Pavlov First Saint Petersburg State Medical University
Email: osa72@inbox.ru
Russian Federation, Saint Petersburg
I. T. Demchenko
Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences
Email: osa72@inbox.ru
Russian Federation, Saint Petersburg
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