目的:研究A型肉毒毒素注射致痉挛瘫痪大鼠腓肠肌及相关结构超微结构的改变。方法:150只大鼠随机分A、B、C、D4组:A组为30只,单纯颅骨钻孔;B组为40只、C组为50只、D组为30只,各组均以适宜电流刺激破坏左侧锥体束制备痉挛瘫痪模型。C组、D组给予腓肠肌痉挛肌肉注射A型肉毒毒素6u/kg/肌群;D组,于注射后辅以运动训练。B组为对照组,给予注射等体积生理盐水。各组于注射后不同时间进行神经行为学检测、肌肉及相关组织结构透射电镜检查。结果:C组和D组的神经、肌肉组织改变情况均较对照B组明显。C组和D组,均观察到神经芽生现象。训练后D组大鼠神经行为学及超微结构改善明显。肌膜两侧呈现不同的病理改变。结论:A型肉毒毒素肌肉注射导致的超微结构改变较单纯肌痉挛造成的改变更为明显;肌细胞膜对肉毒毒素具有阻隔作用,A型肉毒毒素可能有诱发神经芽生作用。运动训练对大鼠神经行为学有明显改善,运动训练可促进病变肌肉超微结构改善。 Objective: To study the ultrastructural changes of gastrocnemius muscle and related structures in spastic paralyzed rats induced by Botulinum Toxin A (Botulinum Toxin A) injection. Methods: One hundred and fifty rats were randomly divided into groups A, B, C and D4: 30 rabbits in group A were scalded with cranium only, 40 rabbits in group B, 50 rabbits in group C and 30 rabbits in group D, Suitable current stimulation to destroy the left pyramidal tract preparation spastic paralysis model. Groups C and D were given gastrocnemius muscle spasm intramuscularly with botulinum toxin type A 6u / kg / muscle; Group D, supplemented with exercise training after injection. Group B as a control group, given an equal volume of saline injection. The neurobehavioral tests were performed at different time points after injection, and the muscle and related tissues were examined by transmission electron microscopy. Results: The changes of nerve and muscle in C group and D group were more obvious than those in control group B. C and D group, were observed in the phenomenon of nerve budding. After training, the neurobehavioral and ultrastructure of rats in group D improved obviously. Muscle membrane showed different pathological changes on both sides. CONCLUSION: The ultrastructural changes caused by intramuscular injection of botulinum toxin A are more obvious than those induced by simple muscle spasm. Muscle cell membranes have a blocking effect on botulinum toxin. Botulinum neurotoxin type A may induce neurite outgrowth. Motor training significantly improved neurological behavior in rats, and exercise training can promote the improvement of the ultrastructure of the diseased muscle.