Effects Of Neurologic Rehabilitation On The Brain Plasticity In Rats With Cerebral Infarction

Part IEffects of Transcranial Magnetic Stimulation (TMS) and Exercisetraining on motor functional recovery after local cerebral infarction inratsObjective To evaluate the effects of TMS and exercise training on motor functional recovery after local cerebral infarction in rats.Methods Experiment one: 36 male SD rats were divided into model group, TMS1 group and TMS2 group randomly (n=12). The rat models of focal cerebral infarction were established with unilateral middle cerebral artery (MCA) suture occlusion method. The rats of TMS1 group were given 0.5Hz, 70% of the maximum output of the stimulator TMS treatment 1 day after infarction (2 times per day, 30 pulses per time) for 4 weeks, the rats of TMS2 group were given 1Hz, 100% of the maximum output of the stimulator TMS treatment 1 day after infarction (2 times per day, 30 pulses per time) for 4 weeks, while those in the control group were reared in their original living state. The neural functions of the three groups were evaluated at 24h, 1w, 2w, 3w and 4weeks after infarction.Experiment two: 48 male SD rats were divided into model group(A), TMS group(B), exercise training group(C) and TMS plus exercise training group(D) randomly (n=12).The rat models of focal cerebral infarction were established with unilateral middlecerebral artery (MCA) suture occlusion method. The rats of TMS group were given0.5Hz, 70% of the maximum output of the stimulator TMS treatment 1 day afterinfarction (2 times per day, 30 pulses per time) for 4 weeks, the rats of exercise traininggroup were given exercise training 1 day after infarction for 4 weeks, the rats of TMSplus exercise training group were given exercise training plus TMS 1 day after infarctionfor 4 weeks, and the rats of model group were reared in their original living state. Theneural functions of the four groups were evaluated at 24 h, 1w, 2w, 3w and 4 weeks afterinfarction.Results Experiment one: The motor function was improved significantly in thetreatment groups as compared with the model group after 3 weeks treatment (P<0.05).but there was no significant difference in the two treatment groups. And there were moreadverse effects in the rats of TMS2 group.Experiment two: The motor function was improved significantly in all treatment groupsas compared with the model group after 3 weeks treatment, especially in the TMS plusexercise training group.Conclusion 1 The 0.5Hz, 70% of the maximum output of the stimulator TMStreatment and 1Hz, 100% of the maximum output of the stimulator TMS treatment couldimprove the motor function in rats after 3 weeks treatment.2 TMS and exercise training could improve the motor function in rat with focal cerebralinfarction. after 3 weeks treatment, and combination of TMS and exercise training havebetter effects than monotherapy.Part IIThe influence of TMS and exercise training on the expressions ofGAP-43 and Syp in rats with focal cerebral infarctionObjective To study the influence of TMS and exercise training on the expressions of GAP-43 and Syp in rats with focal cerebral infarction, so as to explore the material foundation for TMS and exercise training in improving neurorehabilitation.Methods 100 male SD rats were used to focal cerebral infarction model of middle cerebral artery occlusion (MCAO) by intraluminal filament occlusion and then divided into model group(B), TMS group(C), exercise training group(D) and TMS plus exercise training group(E) randomly (n=25). The rats of TMS group were given 0.5Hz, 70% of the maximum output of the stimulator TMS treatment 1 day after infarction (2 times per day, 30 pulses per time) for 4 weeks, the rats of exercise training group were given exercise training 1 day after infarction for 4 weeks, the rats of TMS plus exercise training group were given exercise training plus TMS 1 day after infarction for 4 weeks, and the rats of model group were reared in their original living state. And another 5 male SD rats were put into normal group(A) without operation and treatment. The expressions of GAP-43 and Syp were detected 1d, 3d, 7d, 14d and 28d after MCAO with immunohistochemistry. Results Compared with normal group, GAP-43 immunoreactivity increased at 24 hours after MCAO in the boundary zone of the infarcts in rats after focal cerebral infarction, and reached the peak on the 7^th day, and declined in the later days, but it still remained high level on 28^th day. The expression of GAP-43 were remarkably increased in C, D, and E groups than B group on 7d and 14d, especially in the E group. The expression of Syn was downregulated remarkably in the boundary zone of the infarcts in rats after focal cerebral infarction on 1st day after MCAO, reaching its lowest level at 3d, and slightly increased at 7d. Compared with normal group, Syp immunoreactivity increased on 14d and 28d after MCAO in the boundary zone of the infarcts in rats after focal cerebral infarction. The expression of Syp was remarkably increased in C, D, and E groups than B group on 14d and 28d.Conclusion TMS and exercise training could upregulate the expressions of GAP-43 and Syp in the boundary zone of the infarcts in rats with cerebral infarction, and combination of TMS and exercise training have more effects.Part IIIThe influence of TMS and exercise training on the expression of VEGF and angiogenesis after cerebral infarction in ratsObjective To evaluate the influence of TMS and exercise training on the expressions of VEGF and angiogenesis and its role in functional outcome after cerebral infarction in rats, so as to explore the material foundation for TMS and exercise training in improving neurorehabilitation.Methods 100 male SD rats were used to focal cerebral infarction model of middle cerebral artery occlusion (MCAO) by intraluminal filament occlusion and then divided into model group(B), TMS group(C), exercise training group(D) and TMS plus exercise training group(E) randomly (n=25). The rats of TMS group were given 0.5Hz, 70% of the maximum output of the stimulator TMS treatment 1 day after infarction (2 times per day, 30 pulses per time) for 4 weeks, the rats of exercise training group were given exercise training 1 day after infarction for 4 weeks, the rats of TMS plus exercise training group were given exercise training plus TMS 1 day after infarction for 4 weeks, and the rats of model group were reared in their original living state. And another 5 male SD rats were put into normal group (A) without operation and treatment. The expression of VEGF and angiogenesis was measured in the boundary zone to cerebral infarction at 1d, 3d, 7d, 14d, and 28d after MCAO with immunohistochemistry.Results Compared with normal group, VEGF expression started at 1d after MCAO in the boundary zone of the infarcts in rats after focal cerebral infarction, and subsequently increased, reached peak value at the 3d, failed away until 7d. VEGF expression was mainly detected in the boundary zone of the infarcts at every timepoint. To compare with B group, VEGF expression in C, D, and E groups was significantly increased on 3d and 7d after MCAO, especially in the E group. Compare with control group, the microvessel density (MVD) in rats after focal cerebral infarction were significantly increased in 14d and 28d after MCAO, especially in E group.Conclusion TMS and exercise training could increase the expression and promote the blood vessel proliferation in rats with cerebral infarction, especially in combination treatment of TMS and exercise training.Part IVEffects of Transcranial Magnetic Stimulation (TMS) and exercisetraining on changes of synaptic interface and dendritic structure in the contralateral brain area of rats with cerebral infarctionAbstractObjective To study the effects of transcranial magnetic stimulation (TMS) and exercise training on changes of synaptic interface and dendritic structure in the contralateral brain area of rats with cerebral infarction, to explore the effects of TMS and exercise training on the brain plasticity and its role in functional outcome after cerebral infarction in rats. Methods 32 male SD rats were divided into model group, TMS group, exercise training group and TMS plus exercise training group randomly (n=8). The rat models of focal cerebral infarction were established with unilateral middle cerebral artery (MCA) suture occlusion method. The rats of TMS group were given 0.5Hz, 70% of the maximum output of the stimulator TMS treatment 1 day after infarction (2 times per day, 30 pulses per time) for 4 weeks, the rats of exercise training group were given exercise training 1 day after infarction for 4 weeks, the rats of TMS plus exercise training group were given exercise training plus TMS 1 day after infarction for 4 weeks, and the rats of model group were reared in their original living state. Synaptic and dendritic structure of layer V pyramidal cells within the undamaged motor cortex was assessed morphologically and quantitatively.Results In electron microscopy quantitatively analyzing the synaptic curvatures and post-synaptic density (PSD) were significantly increased, the synapse cleft width was narrower in all treatment group as compared with those of the model group (P < 0.05 or 0.01), and the percentage of perforated synapses in exercise training group and TMS plus exercise training group was significantly increased than those in model group. The synapse cleft width was narrower in TMS plus exercise training group as compared with those in TMS group and exercise training group. Total dendritic length, dendritic branching points and dendritic density of layer V pyramidal cells within the undamaged motor cortex were significantly increased in all treatment groups as compared with those of the model group. And the total dendritic length, dendritic branching points and dendritic density were significantly increased in TMS plus exercise training group as compared with those in TMS group and exercise training group.Conclusion It is postulated that the improved of neural function in rats following TMS are likely to be related to the changes of synaptic and dendritic structure of layer V pyramidal cells within the undamaged motor cortex and increased synaptic plasticity.