S. Yu. Zhilyaev, I. N. Basova, T. F. Platonova, O. S. Alekseeva, N. A. Gavrisheva, I. T. Demchenko
{"title":"Mechanisms of Monoamine Oxidase Involvement in the Development of Hyperbaric Oxygen Seizures","authors":"S. Yu. Zhilyaev, I. N. Basova, T. F. Platonova, O. S. Alekseeva, N. A. Gavrisheva, I. T. Demchenko","doi":"10.1134/s0022093024040161","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Hyperbaric oxygen (HBO<sub>2</sub>) breathing\ninduces generalized tonic and clonic seizures through poorly understood\nmechanisms. The purpose of the research was to evaluate the mechanisms\nof involvement of monoamine oxidase (MAO) in the development of\nhyperbaric oxygen seizures. In rats placed in a pressure chamber\nunder an oxygen pressure of 5 ATA, convulsive reactions were analyzed\nafter the administration of pyrazidol, an MAO-A inhibitor, and pargyline,\nan MAO-B inhibitor. Studies have shown a decrease in the activity\nof MAO isoforms in HBO<sub>2</sub> as well as a delay\nin the development of seizures in animals with inhibition of MAO-A\nand MAO-B. The level of GABA in the brain decreased with HBO<sub>2</sub>,\nand inhibition of MAO-B with pargyline prevented the decrease in\nthe inhibitory transmitter. The results indicate that MAO isoforms\nplay an important role in regulating epileptogenesis in extreme\nhyperoxia. Hyperbaric oxygen, inhibiting the catalytic activity\nof MAO by transforming its molecular structure, leads to disruption\nof the regulation of the exchange of monoamine neurotransmitters\nand a decrease in the level of GABA in the brain, which together\nleads to an imbalance of excitation/inhibition processes in the\ncentral nervous system, which is the basis for the development of oxygen\nepilepsy.</p>","PeriodicalId":0,"journal":{"name":"","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1134/s0022093024040161","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
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 seizures. In rats placed in a pressure chamber
under an oxygen pressure of 5 ATA, convulsive reactions were analyzed
after the administration of pyrazidol, an MAO-A inhibitor, and pargyline,
an 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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