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

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

PO-143 Effects of treadmill exercise on the expression of corticostriatal mGluRs in hemiparkinsonian rats

Objective Exercise therapy has been widely used for the clinical treatment of Parkinson’s Disease (PD). However, the rehabilitation mechanisms involved remain clear. mGluRs play an important role in the progression of PD. In this study, immunohistochemistry and western blot analyses were used to detect the expression of presynaptic corticostriatal mGluR2/3 and postsynaptic mGluR5, and we attempted to investigate the molecular basis of the reconstruction of functional connectivity in the corticostriatal pathways from a mGluR perspective. Methods Male SD rats (230–250 g) were used as subjects in this experiment. After 1 week of habituation, the rats were randomly assigned to three groups: control group (Control, n = 24), PD group (PD, n = 24) and PD with exercise group (PD + Ex, n = 24). The experimental models were prepared by unilateral injection of 6-hydroxydopamine (6-OHDA) (2 μg/L, 8 μg) into the medial forebrain bundle, and the control group was administered an equivalent dose of saline solution. The models were evaluated with the apomorphine (APO)-induced rotation test. Two weeks postoperatively, exercise intervention was applied to the PD + Ex group for 4 weeks. Immunohistochemistry and western blot analysis were used to evaluate the expression of presynaptic corticostriatal mGluR2/3 and postsynaptic mGluR1/5. Results Results showed that the PD + Ex group had a significantly higher level of mGluR2/3 expression (P < 0.01) and significantly lower level of mGluR1/5 expression (P < 0.05) compared with the PD group. Conclusions Exercise intervention significantly increased the expression of mGluR2/3 and simultaneously reduced the expression of mGluR5, indicating that mGluRs can improve the behavioral function of PD rat models through exercise, and that the reconstruction of the functional connectivity of corticostriatal pathways plays an important role in nervous system regulation

PO-187 Exercise reduced the extracellular Glu concentration of striatum neurons in PD model rats by up-regulating mGluR2/3 expression

Objective To investigate the effects of motor intervention on the extracellular Glu concentration and mGluR2/3 mRNA and mGluR2/3 protein expression levels of striatum neurons in PD model rats. Methods Rat model of unilateral injury was established by injecting neurotoxin 6-hydroxydopamine (6-OHDA) into the right brain medial forebrain bundle (MFB)，the sham operation group was given the same dose of normal saline at the same site.Apomorphine (APO) induced rotation behavior test with substantia nigra and striatum TH immunohistochemical staining used to evaluate the reliability of the model. The exercise group began to exercise the treadmill training intervention (11m/min，30min/day，5day/week) at 1 weeks after the operation. Open field experiment and climbing pole experiment used to evaluate the ability of autonomous activity and movement coordination in rats.Western blotting used to detect tyrosine hydroxylase and  mGluR2/3 expression level. RT-PCR was used to detect the expression level of mGluR2 and mGluR3 mRNA in the striatum；In vivo microdialysis combined with high performance liquid chromatography (HPLC) used to detect extracellular Glu concentration in striatal neurons.  Results The results of the microdialysis combined with high performance liquid chromatography (HPLC) showed that，compared with control group，in PD group，Glu concentration of the extracellular of striatal neurons was significantly increased at third and fifth weeks，and the difference was very significant (P<0.01)；Compared with PD group，in PD+Ex group，Glu concentration of the extracellular of striatal neurons was significantly decreased at third and fifth weeks，and the difference was very significant (P<0.05，P<0.01)；Compared with the PD+Ex group，in PD+Ex+ APICA group，Glu concentration of the extracellular of striatal neurons was significantly increased at third and fifth weeks，and the difference was very significant (P<0.05, P<0.01). RT-PCR test results indicated that,the expression level of striatal mGluR3 mRNA of PD group decreased compared with the control group，and the difference was significant (P<0.01)；Compared with the PD group，in the PD+Ex group，the expression level of striatal mGluR3 mRNA increased，a the difference was very significant (P<0.01)；6-OHDA damage and exercise intervention had no effect on the expression of striatum mGluR2 mRNA，and the difference was was not significant (P>0.05). Western blotting results indicated that，the expression level of striatum mGluR2/3 protein of PD group was decreased compared with the control group，and the difference was vey significant (P<0.01)，compared with the PD group，in PD+Ex group，the expression level of striatum mGluR2/3 protein was increased，and the difference significant (P<0.05) . The correlation between the extracellular Glu concentration of the striatum neurons and the total moving distance in PD rats showed that，at third weeks，the extracellular Glu concentration of striatal neurons was negatively correlated with the total movement distance (r=-0.82，P<0.05)，at fifth weeks，the extracellular Glu concentration of striatal neurons was negatively correlated with the total movement distance (r=-0.91，P<0.01). Conclusions The expression level of mGluR2/3 decreased in rats with PD model with increased Gu concentration. The decrease of Gulu concentration and the increase of expression level of mGluR2/3 in the striatum striatum of PD model rats could be induced by the training intervention of running platform, which promoted the improvement of motor dysfunction in PD model rats.&nbsp

PO-056 Endocannabinoid CB1 receptor-mediated abnormal enhancement of rat corticostriatal glutamatergic pathway participates in exercise fatigue Regulation

Objective  By  monitoring the expression of CB1 receptor protein and key regulatory protein RGS4 in the endocannabinoid system (eCBs), and the changes in the transmission efficiency of Corticostriatal glutamatergic pathway and movement ability after microinjection of CB1 receptor agonist WIN 55212-2 into the lateral ventricles in rats, this study  investigates the possible mechanism of striatal eCBs regulation of exercise fatigue. The results may provide experimental basis for further improving the theory of exercise fatigue and  indicate new targets for the regulation of exercise fatigue. Methods 74 adult male Wistar rats were randomly divided into control group (Control) and 1-day fatigue group (1 FG), 3-day fatigue group (3FG) and 7-day fatigue group (7FG) after 3 days rearing. The Control group was in a quiet state and the exercise fatigue group performed exhaustive exercise for 1 day, 3 days and 7 days, respectively. After the induction of exercise fatigue, the expression of CB1 receptor and RGS4 in rat striatum was determined by Western blotting technique. WIN 55212-2 (2mM,5μL)  microinjection into the lateral ventricle plus the stimulation-induced electrophysiological technique was used to determine the effect of CB1 receptor activation  on the evoked spike discharges in striatal MSNs .  Results （1）The results of Western blotting showed that there was no significant change in the expression of CB1 receptor and RGS4 protein in the striatum of rats in 1FG compared with Control group (P＞0.05). But the expression of CB1 receptor and RGS4 in the striatum was significantly increased in both FG and 7FG compared with Control group(P＜0.01). （2）The results of stimulation-induced electrophysiological experiment plus microinjection of lateral ventricle showed that the evoked spike frequency of MSNs in striatum of Control group (2.35±0.66Hz) at 1h after injection of WIN55N212-2 was not significantly different from that before injection (2.43±0.49Hz) (P＞0.05), that the evoked discharge frequency of MSNs in striatum of rats in 1FG（2.63±0.54Hz）was decreased at 10～20min after injection of WIN55N212-2（2.16±0.43Hz）, but no significant difference was found (P＞0.05), that the evoked discharge frequency of MSNs in the striatum of rats in 3FG was decreased at 10～20min after injection of WIN55N212-2（2.16±0.43Hz）, that the evoked discharge frequency of MSNs in the striatum of 3FG（10.57±2.12Hz）was significantly decreased at 10～20min（7.05±1.84Hz）after injection (P＜0.01), and it was basically restored to the pre-injection level by the time of 50～60min injection（10.47±2.83Hz）, and that the evoked discharge frequency of MSNs in the striatum of 7FG（21.7±3.28Hz）was significantly decreased at 10～20min after injection（15.14±1.94Hz）(P＜0.01), and it was basically recovered at 50～60min after injection (19.12±2.89Hz) (P＞0.05). （3）The experimental results of exercise fatigue showed that the time of exercise to fatigue in 7FG group after microinjection of WIN 55-212-2 in lateral ventricle （138.91±8.76min）was significantly longer than that in     artificial cerebrospinal fluid (aCSF) group（127.51±9.45min）(P＜0.05), the time of exercise to fatigue in the 1FG group (105.33±8.99min) was not significantly different from that in the aCSF injection group (105.59±10.34min)（P＞0.05）, the time of exercise to fatigue in 3FG group(118.16±7.99min) was longer than that in aCSF injection group (107.5±10.31min), but there was no statistical significance（P＞0.05）. Conclusions Exercise-induced fatigue could increase the expression of  CB1 receptor protein and key regulatory protein RGS4 in the striatum  and decrease the function of eCBs , which mediated the abnormal enhancement of the transmission efficiency of the corticostriatal glutamatergic pathway and participated in the central regulation of exercise-induced fatigue, and showed an obvious fatigue accumulating effect. The enhancement of the function of eCBs in the striatum of exercise fatigue rats could inhibit the transmission efficiency of rat corticostriatal glutamatergic pathway, and to a certain extent played a role in delaying exercise fatigue. Striatal eCBs may be a new target for central regulation of exercise fatigue

PO-243 Correlation between exercise performance and muscle electrical activity in Exercise-induced Fatigue Rats

Objective Assess the muscle contraction ability of rats before and after exercise fatigue quantitatively, and analyze the correlation between exercise performance and muscle electrical activity. This study intends to provide a theoretical principle for exercise fatigue. Methods 7 healthy adult male SD rats (300~350g) were used and trained for adaptive treadmill by running on the treadmill for 1 week and holding on a vertical rectangular railing (20×10cm, 10 iron bars) until it's mastered. After this training, we used rat grasping force tester( BioSEB GS3) to measure the maximum grasping force(MGF) of rat's limbs, each rat was carried out 3 times, bout interval is 2 minutes. In addition, the grasping bar time(GBT) was recorded 3 times , bout interval is 30 minutes. We let rats to grasp and hold on a vertical rectangular railing(20×10cm， 10 iron bars), evaluation of rat muscular endurance by grasping bar time(GBT), each rat was carried out 3 times, bout interval is 30 minutes; During the MGF and GBT test, motor unit recruitment and discharge frequency was predicted by measuring the EMG of extensor muscles of the right hindlimb and flexor elbow muscles of the right forelimb by wireless non-invasive miniature surface EMG tester (Italy, BTS FREEEMG), the max Root Mean Square (maxRMS) and Median Frequency (MF) parameter was used to evaluate motor unit recruitment and discharge frequency, respectively. After these, the rats were allowed to have a one-day rest, and then had a load motion program on the treadmill (three levels’ load: the first stage movement speed 8.2 m/min, exercise time 15 min; second stage speed 15 m/min, exercise time 15 min; third stage speed at 20 m/min, exercise to fatigue ) to build the rats EF model by monitoring the acceleration of the rat's sprint with a miniature wireless acceleration sensor (18g). 30 continuous sprint acceleration at the end of running was less than half of initial acceleration and the running posture of the rats changed to prostrate, and remained at the end of the runway for a long time. Later, quantitative correlational data analyses such as mean, Pearson correlation, analysis of one-way ANOVA and paired sample t test were performed in this study. Results (1) The rats’ sprint acceleration of treadmill exercise at the end stage (the final 1/5 of the total time) decreased by 56.9% (P < 0.01) when compared with the early stage (the begining 1/5 of the total time). (2) The MGF and GBT of EF decreased by 68.1% (P < 0.01) and 90.38% (P < 0.01), respectively when compared with the beginning EF; in addition, the EMG maxRMS and MF of hindlimb and forelimb of EF rats had significantly reduced (P < 0.01), and the rats’ MGF/GBT was positively correlated with EMG maxRMS/MF significantly (MGF: forelimb rmaxRMS = 0.901, P < 0.01，rMF = 0.761, P < 0.01; hindlimb rmaxRMS = 0.913, P < 0.01，rMF = 0.783, P < 0.01; GBT: forelimb rmaxRMS = 0.922, P < 0.01，rMF = 0.806, P < 0.01; hindlimb rmaxRMS = 0.908, P < 0.01，rMF = 0.896, P < 0.01). Conclusions  Exercise fatigue reduced the muscle strength, muscular endurance and muscle power of rates significantly, which may be related to the decreased recruitment, rhythm synchronization and discharge frequency of muscle motor units of forelimb flexor and hindlimb extensor

PO-134 Optogenetics Active SNc DA Neurons Improve Locomotor Activity on Exercise-Induced fatigue Rats

Objective After optogenetics activing SNc DANs, locomotor activity ability of exercise-induced fatigue rats were recorded to research the role of nigra-striatum DA system in central mechanism of motor control. Methods Used male SD rats (220~240g), randomly divided into 6 groups: sham control group (SCG), optogenetics control group (OCG), fatigue group (FG), sham fatigue group (SFG) and optogenetics fatigue group (OFG). Virus ware injected in the right SNc at coordinates (AP:-5.30 mm, R: 2.00 mm, H-8.00 mm). The SCG/SFG injected 1 μ l saline, OCG/OFG injected 1 μl mixed virus(ChR2 with TH Cre,1:1), the fiber implantation site was deeper than the virus injection about 1 mm. Three weeks after surgery, rats attend 7D exhaustive treadmill exercise. After fatigue running, OCG/OFG/SCG/SFG were in the open field. We used two different light delivery schedules: 10 ms pulses at 20 Hz (10s) and 10 ms pulses at 3 Hz (10s). Sampling time were quiet state, 1D exhaustion, 7D exhaustion and recovery 24h. Animals were euthanized after completion of the behavioral tests. Brains were sectioned coronally in 50-μm slices, images were taken using a fluorescence microscope and determined the anatomical location of the optical fiber. Results (1) OCG/OFG obtain expression of ChR2 in DANs, this was not observed in SCG/SFG; Activation of OCG DANs with 20Hz increased the normalized mean global activity (laser on/laser off), and a significant increment in normalized mean global activity (laser on/laser off) when DANs were activated with 3Hz/20Hz in OFG (p<0.05), showing successful transfection of OCG/OFG. (2) Stimulation at 20 Hz was sufficient to improve global activity, the effects of 3 Hz did not significant, showing 20Hz stimulation possibility be related to motor regulation. (3)The global activity and total distance of rats after 7D exhaustion ware significantly lower than of quiet state (p<0.05), the difference from the quiet state and after 24h recovery is not significant, indicating that the decline in locomotor ability caused by exercise induced-fatigue is reversible. (4) The 20 Hz stimulation significantly improved the global activity of 1D and 7D exhausted rats (p<0.05), indicating that 20 Hz stimulation can effectively improve the rats locomotor activity with exercise-induced fatigue compared with 3 Hz stimulation. Conclusions (1) ChR2 virus transfection can effectively active the nigra-striatum DA system, causing changes in motor performance and increasing the locomotor ability of rats; (2) The locomotor ability of rats with exercise-induced fatigue to decrease. The total distance and global activity decreased significantly with exercise-induced fatigue; (3) Photoactivation of SNc DANs can improve the locomotor activity of rats with exercise-induced fatigue. From the perspective of stimulating effect, 20Hz is the most obvious activation reference point (NSFC: 31401018, SKXJX: 2014014, Corresponding [email protected])

PO-147 Effect of Exercise-induced Fatigue on the Electrical Activity of the External Globus Pallidus Neurons in rats

Objective The motor cortex (MC) stimulation-induced unitary responses of globus pallidus external segment (GPe) neurons in control and exercise induced-fatigue rats were recorded in vivo to examine the role of cortical-striatum-external globus pallidal pathway in the mechanism of central fatigue. Methods 32 Clean healthy male Wistar rats (260~300g), were randomly divided into 4 groups: control group (Control), 1-day fatigue group (1FG), 3-day fatigue group (3FG) and 7-day fatigue group (7FG). Rats were subjected to a 5-day adaptive treadmill training. Modified Bedford treadmill exercise with progressively increasing load was used to creat the exercise fatigue model. （3 levels:8.2 m/min, 15 min; 15m/min, 15 min; 20 m/min, lasting till exhaustion） The spontaneous unit activity and responses to MC stimulation of GPe neurons were recorded by the electrophysiological technique of extracellular recording of glass microelectrodes. Results The results showed that the firing frequency of high-frequency firing with pause (HFP) and low frequency firing with burst (LFB) in the GPe of 1FG was comparable with that of control group (P>0.05). However in 3FG and 7FG , the percentage of HFP neuron was significantly decreased (P<0.05), while the proportion of LFB was significantly increased (P<0.05), and the average firing rate of LFB was higher and inter spike intervals (ISI) was significantly lower than that of the control group. With 200μA electrical stimulation, the explosive discharge of GPe neurons was attenuated after fatigue in rats. The response of GPe neurons to variable frequency stimulation in exhausted model groups was stronger than that of the control group.MC-stimulation typically induced a triphasic response composed of early excitation, inhibition, and late excitation in GPe neurons. The population of neurons showing a short inhibition slightly increased in 3FG and 7FG. Conclusions 1. The results confirmed that GPe is an important nucleus of basal ganglia involved in the regulation of exercise-induced fatigue by the change of spontaneous activity. Electrical stimulation on the cortex can alter response patterns of GPe neurons in exercise-induced fatigue rats, the results confirmed that the Ctx-Str-GPe neural pathway is involved in the regulation of exercise fatigue, and the indirect pathway is over-activated

PL - 022 Effects of exercise-induced fatigue on autonomic activity and dopamine metabolism in rats after D2DR modulation

Objective Objective:  After injection of D2DR antagonist and agonist, the autonomic activity and striatal neurons electrical activity of rats with exercise-induced fatigue were recorded to explore the role of DA receptors in the central mechanism of exercise-induced fatigue. Methods Methods: Used male Wistar rats, randomly divided into 7 groups: control group (CG), one-time exhaustive exercise group (1FG), 3D repetitive exhaust group (3FG), and 7D repetitive exhaustion group (7FG), 7D repeated exhaustive 24h recovery group (24RG) and 7D repeated exhaustive 48h recovery group (48RG). After 1 week adaptive training in rats, rats attend 7D exhaustive treadmill exercise. Subsequently, the autonomic activity changes of each group with D2DR antagonists and agonists were observed in open filed. Used glass microelectrode extracellular recording technique to observe the dorsolateral striatum neurons change of the rats injected with D2DR antagonist spiperone. Real-time PCR (RT-PCR) molecular biology methods were used to measure the expression of D1DR and D2DR in the striatum after exercise-induced fatigue. To investigate the role of DA neurotransmitter and receptor on central mechanism of exercise-induced fatigue. Results Results: (1) With the increase of treadmill exercise load, the total distance of each group became shorter, and the recovery phase gradually recovered to a quiet level. The maximum exercise speed of rats in 7FG was significantly higher than 1FG (P<0.05).The average exercise speed of rats in each group was significantly lower than CG (P<0.05).The average speed of 7FG and 24RG were significantly lower than 1FG(P<0.05). the average movement speed of the 48RG was higher than 7FG;(2) After D2DR antagonist injection, the exhaustive time of rats was significantly lower than CG(P<0.01), while the exhaustive time of D2DR agonist intervention was significantly increased (P<0.01).The active areas of the rats in the open field were concentrated in the corners and margins. The distance of normal rats in 60 min was about 159 m. The activity of rats decreased after D2DR antagonist intervention, the movement distance of rats in CG、1FG and 48RG were significant reduced;(3) After injection of D2DR antagonist, The excitability of dorsolateral striatum neurons were affected by 56.10%, 9.76% (4/41) increased excitability, and 46.34% (19/41) decreased, the inhibitory effect of D2DR agonist was higher than excitatory effects (P<0.05);(4) RT-PCR data showed that there was no significant change in the expression of D1DR in the striatum after exercise-induced fatigue, and D2DR was significantly higher than the CG (P<0.01). Conclusions Conclusion:(1) With the increase of fatigue in rats, the total distance of exercise in each group gradually decreased;(2) Exercise-induced fatigue affects the expression of DA receptors in the striatum;(3) D2DR antagonists and agonists can affect the locomotor ability of rats;(4) D2DR antagonist can inhibit striatal neurons in rats with exercise-induced fatigue, suggesting that D2DR may be one of the drug intervention targets of exercise-induced fatigue.(NSFC: 31401018, SKXJX: 2014014)

Treadmill Exercise Improves Motor Dysfunction and Hyperactivity of the Corticostriatal Glutamatergic Pathway in Rats with 6-OHDA-Induced Parkinson’s Disease

Hyperactivity in the corticostriatal glutamatergic pathway (CGP) induces basal ganglia dysfunction, contributing to parkinsonian syndrome (PS). Physical exercise can improve PS. However, the effect of exercise on the CGP, and whether this pathway is involved in the improvement of PS, remains unclear. Parkinson’s disease (PD) was induced in rats by 6-hydroxydopamine injection into the right medial forebrain bundle. Motor function was assessed using the cylinder test. Striatal neuron (SN) spontaneous and evoked firing activity was recorded, and the expression levels of Cav1.3 and CaMKII in the striatum were measured after 4 weeks of treadmill exercise. The motor function in PD rats was improved by treadmill exercise. SN showed significantly enhanced excitability, and treadmill exercise reduced SN excitability in PD rats. In addition, firing activity was evoked in SNs by stimulation of the primary motor cortex, and SNs exhibited significantly decreased stimulus threshold, increased firing rates, and reduced latency. The expression of Cav1.3 and p-CaMKII (Thr286) in the striatum were enhanced in PD rats. However, these effects were reversed by treadmill exercise. These findings suggest that treadmill exercise inhibits CGP hyperactivity in PD rats, which may be related to improvement of PS

PO-160 Effect of exercise intervention on the synaptic transmission efficiency of cortical-striatum in PD mice

Objective Parkinson's disease (PD) is a neurodegenerative disease caused by degeneration of dopaminergic neurons in the substantia nigra pars compacta and decreased levels of striatal dopamine. Previous studies have confirmed that striatum dysfunction is an important cause of behavioral dysfunction in PD mice, and changes in cortical-striatum synaptic transmission may play an important role in PD pathology. This experiment will use the patch clamp to explore the effect of exercise intervention on the synaptic transmission efficiency of cortical-striatum in PD mice. Methods The experimental animals (C57 mice male, 4 weeks) were randomly divided into normal group(N), PD group(PD)and PD exercise group(PD+EX）.PD mice models were established by injection of 6-OHDA in the striatum (4μg/position, AP + 0.5mm ML - 1.8mm DV - 3.0mm and- 2.0mm). Apomorphine(APO) rotation experiments were performed one week later to identify the model. The formal exercise intervention program was 16m/min, 40min/d, 5d/week,4 weeks（after the adaptive training, total of five weeks of treadmill exercise）. At the end of the intervention, brain slices (350μm) were prepared from each group of mice. The maximum striatum fEPSP (field excitatory postsynaptic potential, fEPSP) and striatum fEPSP under increasing stimulation intensity were recorded. Results 1.The results of APO rotation experiment: PD mice modeled 16/21(205.25±36.46 r higher than the standard). 2.N mice the maximum fEPSP amplitude is 1.9199±0.213mv(n=8)；PD: 1.0129±0.140 mv(n=8); PD+EX: 1.3221±.0865mv(n=8).There are significant differences between groups(P＜0.05). 3. There is a significant decrease in the slope of I-O curve in the PD mice compared with the N mice. And compared with the PD mice, the slope of I-O curve in PD+EX mice was increase(P＜0.05). Conclusions 1. 6-OHDA induced PD model was successfully established. The striatum function was abnormal in the pathological state of PD, and the exercise intervention enhanced the activity of the striatum. 2. The cortical-striatum synaptic transmission efficiency is reduced in the PD state, and the exercise intervention improved the cortical-striatum synaptic transmission efficiency