单胺氧化酶参与高压氧癫痫发作的机制

Pub Date : 2024-08-29 DOI:10.1134/s0022093024040161
S. Yu. Zhilyaev, I. N. Basova, T. F. Platonova, O. S. Alekseeva, N. A. Gavrisheva, I. T. Demchenko
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引用次数: 0

摘要

摘要高压氧(HBO2)呼吸通过不甚明了的机制诱发全身强直和阵挛性癫痫发作。研究的目的是评估单胺氧化酶(MAO)参与高压氧癫痫发作的机制。将大鼠置于氧压为 5 ATA 的压力舱中,分析其在服用 MAO-A 抑制剂吡唑烷醇和 MAO-B 抑制剂帕吉林后的抽搐反应。研究表明,在抑制 MAO-A 和 MAO-B 的情况下,HBO2 中 MAO 同工酶的活性会降低,动物癫痫发作的时间也会推迟。脑内 GABA 的水平随 HBO2 而下降,而用帕吉林抑制 MAO-B 可以防止抑制性递质的下降。这些结果表明,MAO 同工酶在极度缺氧时调节癫痫发生中发挥着重要作用。高压氧通过改变 MAO 的分子结构来抑制 MAO 的催化活性,从而导致单胺类神经递质交换的调节紊乱和脑内 GABA 水平的下降,这共同导致了中枢神经系统兴奋/抑制过程的失衡,而这正是氧性癫痫发生的基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Mechanisms of Monoamine Oxidase Involvement in the Development of Hyperbaric Oxygen Seizures

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Mechanisms of Monoamine Oxidase Involvement in the Development of Hyperbaric Oxygen Seizures

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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