ABSTRACT
Objective To explore the effects of excise-induced fatigue on the microloop plasticity of prefrontal cortex through observing the expression of parvalbumin positive neurons in prefrontal cortexes of rats induced by exhaustive exercise,so as to find out the possible mechanism of the central regulation of exercise-induced fatigue by measuring the expression of NMDAR2B receptors.Methods Thirty-six Wistar rats were randomly divided into an exhausted group (E),a repeated exhaustion group (RE) and a control group (CG),each of 12.For group E,the adjusted Bedford incremental load of treadmill exercise program was employed:the initial treadmill speed was 8.2 m/min,lasting for 15 minutes,then increased to 15 m/min for another 15 minutes,and finally increased to 20 m/min till exhaustion.For RE group,they were given continuous treadmill exercises to exhaustion for consecutive 7 days.The immunofluorescence technique was used to observe the expression of PV+ interneurons after exhausted treadmill running.The Western blotting technique was used to determine the expression of NMDAR2B in the tissue of the prefrontal cortex.Results After the exhausted treadmill running,the expression of PV+ interneurons in the prefrontal cortexes of both E and RE groups increased significantly compared with the control group(P＜0.01).The immunofluorescence results indicated that NMDAR2B positive neurons were seen in group E,but not obviously in group CG and RE.The Western blotting showed that compared with CG group the protein expression of NMDAR2B in prefrontal cortexes of group E was relatively high,and that of group RE was relatively low,but without significant difference (P＞0.05).The running distance and prefrontal cortex NMDAR2B expression were found negatively correlated (P＜ 0.01).Conclusions Exhaustive exercises have an impact on the plasticity in rats' prefrontal cortex neural network through regulating the local loop of PV positive neurons.This plasticity of the prefrontal cortex is involved in the regulation of central fatigue.The present study might provide morphological basis for the research of central mechanism of the exercise-induced fatigue.