The anticonvulsant effects of salmon calcitonin on pentylenetetrazole-kindled rats

Q4 Biochemistry, Genetics and Molecular Biology

Journal of Cellular Neuroscience and Oxidative Stress Pub Date : 2019-06-21 DOI:10.37212/JCNOS.584705

A. Taskiran, E. Ozdemir

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Abstract

Epilepsy is a disorder of the brain, characterized by an enduring predisposition for the generation of epileptic seizures because of hyperexcitability and hypersynchrony of cortical neurons (Devinsky et al. 2014). Salmon calcitonin is a type of calcitonin with 32 amino acids. It is more potency than human calcitonin due to differences in its amino acid sequence (Masi et al. 2007). In the current study, we investigated the effects of salmon calcitonin on pentylenetetrazoleinduced seizures in kindled rats. In our study, 48 (240-260 g) male Wistar Albino rats were used. Rats were kindled by injections of a subconvulsant dose of pentylenetetrazole (35 mg/kg) once every other day for 15 times. Epileptic behaviors were observed for a period of 30 min. Seizure activity was scored, using the revised Racine’s scale. Rats that had seizure stages of 4 or 5 after three consecutive injections of PTZ were defined as fully kindled. The kindled rats were divided into six groups (n=8 for each group) as saline (1 ml/kg saline), salmon calcitonin (25, 50 and 100 µg/kg), ethosuximide (100 mg/kg) and ethosuximide + salmon calcitonin. Electrodes were placed to animals’ skulls under stereotaxy to receive electroencephalography (EEG). After thirty minutes of administration of drugs, 35 mg/kg PTZ was given to induce seizures. EEG and video recordings of animals were taken simultaneously for thirty minutes. In the evaluation of the video and EEG recordings, the seizure stages of animals, the first myoclonic jerk time and the number of epileptic seizure spikes were calculated. Salmon calcitonin reduced seizures stage, epileptic seizure spikes and also prolonged first myoclonic jerk time compared to saline group. In addition, salmon calcitonin and ethosuximide combination decreased epileptic seizure spikes and increased the first myoclonic jerk time compare to ethosuximide group. In conclusion, salmon calcitonin decreased epileptic seizures and improved anticonvulsant effect of ethosuximide in the pentylentetrazole-kindled rat.

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鲑鱼降钙素对戊四唑点燃大鼠的抗惊厥作用

癫痫是一种大脑疾病，其特征是由于皮层神经元的超兴奋性和超同步性，长期易发生癫痫发作（Devinsky等人，2014）。鲑鱼降钙素是一种含有32个氨基酸的降钙素。由于其氨基酸序列的差异，它比人类降钙素更有效力（Masi等人，2007）。在本研究中，我们研究了鲑鱼降钙素对点燃大鼠戊四氮诱导的癫痫发作的影响。在我们的研究中，使用了48只（240-260g）雄性Wistar Albino大鼠。大鼠通过每隔一天注射一次亚惊厥剂量的戊四唑（35mg/kg）点燃，共15次。癫痫行为观察持续30分钟。使用修订的拉辛量表对癫痫活动进行评分。连续三次注射PTZ后癫痫发作阶段为4或5的大鼠被定义为完全点燃。将点燃的大鼠分为六组（每组n=8），分别为生理盐水（1 ml/kg生理盐水）、鲑鱼降钙素（25、50和100µg/kg）、乙硫胺（100 mg/kg）和乙硫胺+鲑鱼降钙剂。在立体定向下将电极放置在动物的头骨上以接收脑电图（EEG）。给药30分钟后，给予35mg/kg PTZ以诱导癫痫发作。动物的脑电图和视频记录同时进行了30分钟。在对视频和脑电图记录的评估中，计算了动物的癫痫发作阶段、第一次肌阵跳时间和癫痫发作棘波的数量。与生理盐水组相比，鲑鱼降钙素降低了癫痫发作阶段、癫痫发作高峰，并延长了首次肌阵挛抽搐时间。此外，与乙磺酰亚胺组相比，鲑鱼降钙素和乙磺酰肟联合用药降低了癫痫发作高峰，并增加了第一次肌阵跳时间。总之，鲑鱼降钙素降低了戊四唑点燃大鼠的癫痫发作，并改善了乙磺酰亚胺的抗惊厥作用。

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)