The role of 5-HT3 receptor antagonist on the gene expression 5-HT3a in the electrical amygdala kindled rats

سال انتشار: 1398
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 443

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شناسه ملی سند علمی:

NSCMED08_500

تاریخ نمایه سازی: 15 دی 1398

چکیده مقاله:

Background and Aim : Epilepsy is a brain disorder characterized by the recurrence of otherwise unprovoked seizures, that is, by an enduring predisposition to generate seizures and by the neurobiological, cognitive, psychological, and social consequences of this condition. The definition of epilepsy requires the occurrence of at least one seizure. Among the different types of epilepsy, temporal lobe epilepsy is the most prevalent and its most commonly used animal model is kindling. In the kindling model of epilepsy, repeated electrical stimulation of a target brain area induces permanently enhanced seizure susceptibility and other enduring brain alterations that are similar to those occurring in human temporal lobe epilepsy. The amygdala is one of the most sensitive areas for the induction of kindled seizures.The aim of this study was to determine the role of 5-HT3 receptor antagonist on the gene expression 5-HT3a in the electrical amygdala kindled rats.Methods : Male Wistar rats (weighing 270–350 g) were used in this study. Animals were assigned to seven groups as control, sham, kindled, kindled + vehicle, kindled + Ramo. 1μg, kindled + Ramo. 10μg, kindled + Ramo. 100μg. In kindled + vehicle group, animals were injected with ramosetron vehicle and then received the kindling stimulations. In kindled + Ramo. 1 μg group, animals were injected with ramosetron 1μg / 0.5 μl (ICV) and then received the kindling stimulations 24 h after applying the vehicle injection. In kindled + Ramo. 10 μg group, animals were injected with ramosetron 10 μg / 0.5 μl (ICV) and then received the kindling stimulations 24 h after applying the vehicle injection. In kindled + Ramo. 100 μg group, animals were injected with ramosetron 100μg / 0.5 μl (ICV) and then received the kindling stimulations 24 h after applying the vehicle injection. For quantitative real time-PCR (qRT-PCR), animals were sacrificed and their hippocampus were extracted immediately after Conduct behavioral tests.Results : Main findings: 1) The 5-HT3a gene expression in Kindled and Kindled + vehicle groups compared with the control group and low and moderate doses compared with high doses was significantly reduced. 2) The 5-HT3a gene expression in moderate dose compared with Kindled and Kindled + vehicle groups increased significantly. 3) The 5-HT3a gene expression in high dose compared with control, Kindled and Kindled + vehicle groups increased significantly.Conclusion : The results of our study show that the expression level of 5-HT3a gene in kindle and kindle + vehicle groups was decreased compared to the control and low and medium dose drug groups compared to the high dose group, whereas Medium and high dose recipients were significantly increased compared to the Kindle and Kindle + vehicle groups.Previous findings showed that Cx30 mRNA expression was increased at the start of kindling and after focal seizures, and that when animals received general seizures, gene expression decreased. The increase in Cx30 mRNA expression at the start of kindling is inconsistent with the initial increase in the corresponding protein.

نویسندگان

Zeinab Sayyahi

Department of Physiology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran-Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran

Mohammad Sadegh Bolandian

Department of Physiology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran-Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran

Javad Mirnajafi-zadeh

Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran

Abdolrahman Sarihi

Department of Physiology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran-Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran

Alireza Komaki

Department of Physiology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran-Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran

Masoud Saeidi Jam

Department of Molecular Medicine and Genetics, Hamadan University of Medical Sciences, Iran