Faculty of Medicine, Department of Biophysics, Yozgat Bozok University, 66100 Yozgat, Turkey.
Medical Faculty, Yozgat Bozok University, 66100 Yozgat, Turkey.
Life Sci. 2021 Jan 15;265:118826. doi: 10.1016/j.lfs.2020.118826. Epub 2020 Nov 28.
Epilepsy is a neurologicaldisorder characterized by persistent predisposition to recurrent seizurescaused by abnormal neuronal activity in the brain. Epileptic seizures maydevelop due to a relative imbalance of excitatory and inhibitory neurotransmitters. Expressional alterations of receptors and ion channelsactivated by neurotransmitters can lead to epilepsy pathogenesis.
In this updated comprehensive review, we discuss the emerging implication of mutations in neurotransmitter-mediated receptors and ion channels. We aim to provide critical findings of the current literature about the role of neurotransmitters in epilepsy.
A comprehensive literature review was conducted to identify and critically evaluate studies analyzing the possible relationship between epilepsy and neurotransmitters. The PubMed database was searched for related research articles.
Glutamate and gamma-aminobutyric acid (GABA) are the main neurotransmitters playing a critical role in the pathophysiology of this balance, and irreversible neuronal damage may occur as a result of abnormal changes in these molecules. Acetylcholine (ACh), the main stimulant of the autonomic nervous system, mediates signal transmission through cholinergic and nicotinic receptors. Accumulating evidence indicates that dysfunction of nicotinic ACh receptors, which are widely expressed in hippocampal and cortical neurons, may be significantly implicated in the pathogenesis of epilepsy. The dopamine-norepinephrine-epinephrine cycle activates hormonal and neuronal pathways; serotonin, norepinephrine, histamine, and melatonin can act as both hormones and neurotransmitters. Recent reports have demonstrated that nitric oxide mediates cognitive and memory-related functions via stimulating neuronal transmission.
The elucidation of the role of the main mediators and receptors in epilepsy is crucial for developing new diagnostic and therapeutic approaches.
癫痫是一种以大脑神经元异常活动为特征的神经系统疾病，表现为反复发作的倾向。癫痫发作可能是由于兴奋性和抑制性神经递质之间的相对失衡引起的。神经递质激活的受体和离子通道的表达改变可导致癫痫发病机制。
在本次更新的全面综述中，我们讨论了递质介导的受体和离子通道突变的新出现意义。我们旨在提供有关神经递质在癫痫中的作用的当前文献的关键发现。
进行了全面的文献综述，以确定和批判性评估分析癫痫与神经递质之间可能关系的研究。在 PubMed 数据库中搜索了相关的研究文章。
谷氨酸和γ-氨基丁酸（GABA）是主要的神经递质，在这种平衡的病理生理学中起着关键作用，并且这些分子的异常变化可能导致不可逆的神经元损伤。乙酰胆碱（ACh）是自主神经系统的主要刺激物，通过胆碱能和烟碱型受体介导信号传递。越来越多的证据表明，广泛表达于海马和皮质神经元中的烟碱型 ACh 受体功能障碍可能与癫痫发病机制密切相关。多巴胺-去甲肾上腺素-肾上腺素循环激活激素和神经元途径；血清素、去甲肾上腺素、组胺和褪黑素既可以作为激素，也可以作为神经递质。最近的报告表明，一氧化氮通过刺激神经元传递来介导认知和记忆相关功能。
阐明癫痫中主要介质和受体的作用对于开发新的诊断和治疗方法至关重要。
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