TRPV1 channel is a potential drug discovery channel for epilepsy

Q4 Biochemistry, Genetics and Molecular Biology

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2018-08-18 DOI:10.37212/JCNOS.610113

Ahmet Özşimşek

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Abstract

Epilepsy is one of the most frequent and heterogeneous neurological disorders and it is characterized by several disabilities. Epilepsy is affecting about 3% of people worldwide. Current antiepileptic drugs are only effective in 60% of individuals and many drugs can induce several unwanted side effects in patients. Etiology of epilepsy has not been clarified fully. However, increased intracellular calcium ion (Ca 2+ ) concentration has main role in etiology of epilepsy. Ca2+ passes the cell membrane through different cell membrane channels. One of the channels is TRP superfamily. The family is containing six subfamilies. TRPV1 channel is a member of TRPV subfamily. Capsaicin is a component of hot chili pepper. The TRPV1 channels is activated by different stimuli such as acidic pH, high temperature (≥ 42° C) and capsaicin, causing pain, inflammation and hyperalgesia in peripheral nervous system (Caterina et al. 1997). Is has been well known that hippocampus is main area in the brain for induction of epilepsy. Expression levels of TRPV1 channels in different areas of hippocampus are high (Gonzalez-Reyes et al. 2013). Results of recent studies indicated involvement of TRPV1 channels in epilepsy (Naziroglu and Ovey, 2015; Cho et al. 2018). In the oral presentation, I discussed novel roles of TRPV1 on the epilepsy induction by the capsaicin. Results of a recent study indicated increased levels of intracellular Ca2+ concentration in hippocampus of epilepsy induced rats (Naziroglu and Ovey, 2015). They also observed increased levels of intracellular mitochondrial oxidative stress and apoptosis levels in the neurons by the capsaicin stimulation. However, their levels were decreased by inhibition of TRPV1 channel blocker, capsazepine. I concluded that the results of recent studies suggest that TRPV1 stimulation through capsaicin causes oxidative stress and intracellular Ca2+ signaling in epileptic rats. It seems to that the certain role of TRPV1 channel activation in in the epilepsy still remains to be determined.

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TRPV1通道是一个潜在的癫痫药物发现通道

癫痫是最常见和异质性的神经系统疾病之一，其特点是几种残疾。全世界约有3%的人患有癫痫。目前的抗癫痫药物仅对60%的个体有效，而且许多药物会对患者产生一些不想要的副作用。癫痫的病因尚未完全清楚。然而，细胞内钙离子(ca2 +)浓度升高在癫痫发病中起主要作用。Ca2+通过不同的细胞膜通道通过细胞膜。其中一个通道是TRP超家族。这个科包含六个亚科。TRPV1通道是TRPV亚族的成员。辣椒素是辣椒的一种成分。TRPV1通道被酸性pH、高温(≥42℃)和辣椒素等不同刺激激活，引起周围神经系统疼痛、炎症和痛觉过敏(Caterina et al. 1997)。众所周知，海马体是大脑中诱发癫痫的主要区域。TRPV1通道在海马不同区域的表达水平较高(Gonzalez-Reyes et al. 2013)。最近的研究结果表明，TRPV1通道参与癫痫(Naziroglu和Ovey, 2015;Cho et al. 2018)。在口头报告中，我讨论了TRPV1在辣椒素诱导癫痫中的新作用。最近的一项研究结果表明，癫痫诱导大鼠海马细胞内Ca2+浓度水平升高(Naziroglu和Ovey, 2015)。他们还观察到，在辣椒素刺激下，神经元细胞内线粒体氧化应激水平和细胞凋亡水平增加。然而，它们的水平通过抑制TRPV1通道阻滞剂capsazepine而降低。我的结论是，最近的研究结果表明，通过辣椒素刺激TRPV1会引起癫痫大鼠的氧化应激和细胞内Ca2+信号传导。似乎TRPV1通道激活在癫痫中的作用仍有待确定。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Cellular Neuroscience and Oxidative Stress Biochemistry, Genetics and Molecular Biology-Biophysics

CiteScore

1.10

自引率

0.00%

发文量

期刊介绍： Journal of Cellular Neuroscience and Oxidative Stress isan online journal that publishes original research articles, reviews and short reviews on themolecular basisofbiophysical,physiological and pharmacological processes thatregulate cellular function, and the control or alteration of these processesby theaction of receptors, neurotransmitters, second messengers, cation, anions,drugsor disease. Areas of particular interest are four topics. They are; 1. Ion Channels (Na+-K+Channels, Cl– channels, Ca2+channels, ADP-Ribose and metabolism of NAD+,Patch-Clamp applications) 2. Oxidative Stress (Antioxidant vitamins, antioxidant enzymes, metabolism of nitric oxide, oxidative stress, biophysics, biochemistry and physiology of free oxygen radicals) 3. Interaction Between Oxidative Stress and Ion Channels in Neuroscience (Effects of the oxidative stress on the activation of the voltage sensitive cation channels, effect of ADP-Ribose and NAD+ on activation of the cation channels which are sensitive to voltage, effect of the oxidative stress on activation of the TRP channels in neurodegenerative diseases such Parkinson’s and Alzheimer’s diseases) 4. Gene and Oxidative Stress (Gene abnormalities. Interaction between gene and free radicals. Gene anomalies and iron. Role of radiation and cancer on gene polymorphism)