OR-034 The parvalbumin positive neuron involved the regulation of motor cortex excitability in the exercise-induced fatigue

Shuqiang Cui, D. Qiao, Xiaoli Liu
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Abstract

Objective Objective:Cortical parvalbumin-expressing inhibitory neurons(PV) control the activity of excitatory neurons and regulate their spike output. The present experiment is to determine the role of PV neuron in the reglution of excitability of primary motor cortex (M1) during the exercise-induced fatigue and possible molecular mechanism. Methods Methods: Male Wistar rats randomly divided into control group(C),exhaustive exercise group(E) and repeated exhaustive exercise group(RE). The gradually increasing load treadmill exercise-induced fatigue model was employed in the Group E and RE.The in vivo multi-channel recording methods was used for recording the neuronal electrophysiological activities of primary motor cortex.To observe the neuron firing rate changes during the rest state,immediately after exhausted exercise and after repeated exhaustive exercise.We also detected the expression of PV positive neurons in the primary motor cortex by the immunofluorescence method. The western blot method was used to determine the expression of calmodulin-dependent protein kinase II (CaMKII)、phosphorylated calmodulin-dependent protein kinase II( pCaMKII) and extracellular signal regulated kinase (ERK) in the primary motor cortex. Results Results:The electrophysioligical results indicated that the neuron firing rate after repeated exhausted excise the neuron firing rate significantly decreased compared with the rest state (P<0.05),but have no significantly changes as compared with exhausted excise;The expression of PV positive neurons in the group of E and RE significantly increased compared with the group C(P<0.01);The western blot results indicated that the protein expression of ERK in group REsignificantly decreased compared with group C, the pCaMKII expression of group RE decreased,but have no statistical difference. Conclusions Conclusion: After exercise-indued fatigue ,the increase of PV positive neuron maybe one reason for the excitability changes in primary motor cortex.the alteraions in the electrical signal may be participate in the regluation of exercise-induced fatigue. pCaMKII and ERK signal pathway may invloved in the molecular mechanism of exercise-induced fatigue.
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在运动性疲劳中,小白蛋白阳性神经元参与运动皮层兴奋性的调节
目的目的:皮层小蛋白表达抑制神经元(PV)控制兴奋性神经元的活动并调节其峰输出。本实验旨在探讨PV神经元在运动性疲劳过程中对初级运动皮层(M1)兴奋性的调控作用及其可能的分子机制。方法:雄性Wistar大鼠随机分为对照组(C)、力竭运动组(E)和重复力竭运动组(RE)。E组和re组采用负荷逐渐增加的跑步机运动性疲劳模型,采用体内多通道记录法记录初级运动皮层神经元电生理活动。观察静息状态下、疲劳运动后及反复疲劳运动后神经元放电速率的变化。免疫荧光法检测原发性运动皮层PV阳性神经元的表达。western blot法检测原代运动皮层钙调素依赖性蛋白激酶II(CaMKII)、磷酸化钙调素依赖性蛋白激酶II(pCaMKII)和细胞外信号调节激酶(ERK)的表达。结果结果:电生理结果显示,重复竭电切除后神经元放电率与静息状态相比显著降低(P<0.05),但与竭电切除相比无显著变化;E组和RE组PV阳性神经元表达较C组显著升高(P<0.01); western blot结果显示,RE组ERK蛋白表达较C组显著降低C组,RE组pCaMKII表达降低,但差异无统计学意义。结论:运动性疲劳后,PV阳性神经元的增加可能是原代运动皮层兴奋性改变的原因之一。电信号的改变可能参与了运动性疲劳的调节。pCaMKII和ERK信号通路可能参与运动性疲劳的分子机制。
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