癫痫患者松果体的超微结构变化

Tetyana Litovchenko, Andrey Dubenko, Serhii Sazonov, V. Florikian, Olena Zavalna, Olga Sukhonosova
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引用次数: 0

摘要

昼夜节律机制在多个层面上调节神经元的兴奋性,破坏昼夜节律机制会导致兴奋性过度失控。以往的研究表明,癫痫与褪黑激素水平有关。褪黑激素是松果体分泌的一种强效时间生物素,有助于维持正常的昼夜节律,并可用于治疗某些神经和精神疾病。昼夜节律和睡眠/觉醒机制在癫痫中发挥作用。缺乏褪黑激素会降低癫痫发作阈值,从而增加癫痫发作活动。本研究旨在确定癫痫实验模型中松果体的超微结构变化。材料和方法实验对象为 Wistar 大鼠,5-6 个月大,体重约 200 克,实验组 36 只,对照组 10 只。再现了大鼠电刺激实验性癫痫发作模型。大鼠在受到 9-14 次刺激后出现自发性全身抽搐。用于组织学检查的材料是在反复癫痫发作稳定(超过 1 个月)后采集的。超薄切片经柠檬酸雷诺铅对比后,在电子显微镜下以 75 千伏的加速电压进行研究。加速度根据研究需要选择,范围在 20,000 至 60,000 倍之间。研究结果实验研究证实,在大鼠癫痫实验模型中,松果体存在稳定的萎缩,甚至部分细胞凋亡,松果体的形态发生了变化,这是松果体功能活性下降的原因。结论我们关于松果体形态变化的实验数据证实了癫痫患者松果体功能的稳定下降(可能是不可逆的)是由松果体细胞结构的损伤和破坏造成的这一结论。鉴于褪黑激素的多功能性,它的缺乏可能是神经网络发生变化、突触膜通透性受损以及神经元癫痫活动增加的原因之一。
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ULTRASTRUCTURAL CHANGES OF THE PINEAL GLAND IN EPILEPSY
Circadian mechanisms modulate neuronal excitability at several levels, and their destruction can cause excessive uncontrolled excitability. Previous studies have shown that epilepsy is associated with melatonin levels. Melatonin is a powerful chronobiotic secreted from the pineal gland; helps to maintain normal circadian rhythms and is used to treat some neurological and psychiatric disorders. Circadian rhythms and sleep/wake mechanisms play role in the epilepsy. Melatonin deficiency can decrease seizure threshold, and hence could increase seizure activity. The aim of the study was to identify ultrastructural changes in the pineal gland in an experimental model of epilepsy. Materials and methods. The experiment was carried out on Wistar rats, 5-6 months of age, weight of about 200 g, 36 experimental and 10 control animals. Electrically provoked experimental epileptic seizures model in rats was reproduced. The rats developed spontaneous generalized seizures after 9-14 stimulations. Material for histological examinations was taken after stable formation (for >1 month) of repeated seizures. Ultrathin sections, after contrast with Reynolds lead citrate, were studied under an electron microscope at an accelerating voltage of 75 kV. The increase was selected adequate to the study and ranged from 20,000 to 60,000 times. Results. Experimental studies have confirmed the presence of stable dystrophic, up to apoptosis of some cells, morphological changes of the pineal gland in the experimental model of epilepsy in rats, which is the reason for the decrease in its functional activity. Conclusions. Our experimental data on the morphological changes of the pineal gland confirm the conclusion about a stable, possibly irreversible, decrease in gland function in epilepsy due to damage and disruption of the structure of its cells. Given the polyfunctionality of melatonin, its deficiency can be one of the causes of changes in neural networks, impaired permeability of synaptic membranes, and as a consequence, increased epileptic activity of neurons.
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