Lim Baek-Vin, Shin Mal-Soon, Lee Jae-Min, Seo Jin-Hee
Department of Exercise Prescription, Division of Leisure & Sports Science, Dongseo University, Busan, Korea.
Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea.
J Exerc Rehabil. 2015 Apr 30;11(2):80-6. doi: 10.12965/jer.150193. eCollection 2015 Apr.
Epilepsy is a common neurological disorder characterized by seizure and loss of neuronal cells by abnormal rhythmic firing of neurons in the brain. In the present study, we investigated the effect of treadmill exercise on gamma-aminobutyric acid (GABA)ergic neuronal loss in relation with neuronal activation using pilocarpine-induced epileptic rats. The rats were divided into four groups: control group, control and treadmill exercise group, pilocarpine-induced epilepsy group, and pilocarpine-induced epilepsy and treadmill exercise group. Epilepsy was induced by intraperitoneal injection of 320 mg/kg pilocarpine hydrochloride. The rats in the exercise groups were forced to run on a motorized treadmill for 30 min once a day for 2 weeks. In the present results, neuronal loss in the hippocampal CA1 region was increased after pilocarpine-induced seizure. Treadmill exercise inhibited hippocampal neuronal loss in the epileptic rats. Glutamic acid decarboxylase (GAD67) expression in the hippocampal CA1 region was reduced by pilocarpine-induced seizure. Treadmill exercise increased GAD67 expression in the epileptic rats. c-Fos expression in the hippocampal CA1 region was increased in response to epileptic seizure. Treadmill exercise inhibited c-Fos expression in the epileptic rats. Epileptic seizure increased brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB) expressions in the hippocampus. Treadmill exercise suppressed BDNF and TrkB expressions in the epileptic rats. In the present study, treadmill exercise prevented GABAergic neuronal loss and inhibited neuronal activation in the hippocampal CA1 region through the down-regulation of BDNF-TrkB signaling pathway.
癫痫是一种常见的神经系统疾病，其特征为癫痫发作以及大脑中神经元异常节律性放电导致神经元细胞丧失。在本研究中，我们使用毛果芸香碱诱导的癫痫大鼠，研究了跑步机运动对γ-氨基丁酸（GABA）能神经元丧失以及与神经元激活之间关系的影响。大鼠被分为四组：对照组、对照组及跑步机运动组、毛果芸香碱诱导癫痫组、毛果芸香碱诱导癫痫及跑步机运动组。通过腹腔注射320mg/kg盐酸毛果芸香碱诱导癫痫。运动组的大鼠每天被迫在电动跑步机上跑30分钟，持续2周。在本研究结果中，毛果芸香碱诱导癫痫发作后，海马CA1区的神经元丧失增加。跑步机运动抑制了癫痫大鼠海马神经元的丧失。毛果芸香碱诱导癫痫发作使海马CA1区谷氨酸脱羧酶（GAD67）表达降低。跑步机运动增加了癫痫大鼠GAD67的表达。癫痫发作使海马CA1区c-Fos表达增加。跑步机运动抑制了癫痫大鼠c-Fos的表达。癫痫发作增加了海马中脑源性神经营养因子（BDNF）和酪氨酸激酶受体B（TrkB）的表达。跑步机运动抑制了癫痫大鼠BDNF和TrkB的表达。在本研究中，跑步机运动通过下调BDNF-TrkB信号通路，预防了GABA能神经元丧失并抑制了海马CA1区的神经元激活。
