[Effects of transcranial magnetic stimulation on recovery of neural functions and changes of synaptic interface and dendritic structure in the contralateral brain area after cerebral infarction: experiment with rats].

Objective To evaluate the effects of transcranial magnetic stimulation(TMS)on the brain plasticity and its role in functional outcome in cerebral infarction.Methods Twenty male SD rats underwent suture of the unilateral middle cerebral artery(MCA)so as to establish focal cerebral infarction models and then were randomly divided into 2 equal groups:model group,to be reared in the original living state,and TMS group,given in addition TMS treatment 1 day after infarction 2 times per day and 30 pulses per time for 4 weeks.Twenty-eight days after the rats were killed.Four rats from each group underwent microscopy of the brain to measure the dendritic structure of the pyramidal cells quantitatively.Other 4 rats from each group underwent electron microscopy of the brain to measure the parameters of synaptic interface in the sensorimotor cortex.Neural function scoring was conducted 24 hours after the establishment of model and before being killed.Results There was no significant difference in the neural function 24 h after the establishment of models,however,28 days after the score of neural function of the TMA group was 0.58± 0.49,significandy lower than that of the model group(0.92±0.28,P0.05).The total dendritic length, number of dendritic branching points,and dendritic density in layer V pyramidal cells within the undamaged motor cortex of the TMS group were 898μm±127μm,6.6±1.5,and 0.75/μm±0.19/μm,all significantly higher than those of the model group(788μm±112μm,5.8±1.5,and 0.60/μm±0.16/ μm,P0.05 or0.01).Electron microscopy showed that the synaptic curvatures and post-synaptic density of the TMS group were 1.06±0.08 and 64±13 respectively,both significantly higher than those of the model group(1.02±0.06 and 54±12 nm respectively,P0.05 and P0.01),and the synapse cleft width of the TMS group was 19.5±2.1,significantly narrower than that of the model group(23.3±2.3,P 0.01).Conclusion TMS promotes the improvement of neural functions of the rats with cerebral ischemia by the potential mechanism that TMS strengthen the compensatory roles of the synaptic interface and dendritic structure in the undamaged sensorimotor cortex area and increase svnaptic plasticity.