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目的:通过观察运动干预对PD模型大鼠纹状体突触超微结构、Glu浓度、D2DR及NMDAR1表达的影响,揭示运动调节PD大鼠皮层-纹状体Glu能神经传递的机制。方法:选用清洁级雄性SD大鼠,随机分为假手术安静组、假手术运动组、帕金森安静组、帕金森运动组,每组18只。采用6-OHDA于内侧前脑束单点注射建立PD大鼠模型,假手术组给予同等剂量生理盐水。术后24 h对运动组大鼠进行运动干预,运动方案为11 m/min,30 min/d,5 d/周,4周。采用透射电子显微镜技术观察皮层-纹状体突触的超微结构,高效液相色谱法(HPLC)检测纹状体Glu浓度,免疫组化与免疫印迹技术观察纹状体D2DR及NMDAR1表达变化。结果:PD运动组大鼠纹状体穿通型突触占不对称突触的比例较PD组明显降低(P<0.05)。PD运动组大鼠纹状体Glu浓度较PD组显著下降(P<0.01)。PD运动组大鼠纹状体D2DR与NMDAR1的表达较PD组显著增加(P<0.05,P<0.05)。结论:运动干预改善了PD模型大鼠皮层-纹状体Glu能神经传递效能,可能与DA对Glu能突触活性的调节作用增强有关。
OBJECTIVE: To observe the effect of exercise intervention on synaptic ultrastructure, Glu concentration, D2DR and NMDAR1 expression in striatum of PD rats and to reveal the mechanism of exercise-induced glutamate neurotransmission in cortex and striatum. Methods: Clean male Sprague-Dawley rats were randomly divided into sham operation group, sham operation group, Parkinson’s quiet group and Parkinson’s exercise group, with 18 rats in each group. PD rats were established by single injection of 6-OHDA in the medial forebrain. The rats in the sham operation group were given the same dose of normal saline. The rats in exercise group were exercised 24 hours after exercise, and the exercise program was 11 m / min, 30 min / d, 5 d / week and 4 weeks. The ultrastructure of cortical-striatum synapses was observed by transmission electron microscopy. Glu levels in striatum were detected by high performance liquid chromatography (HPLC). The expression of D2DR and NMDAR1 in striatum was observed by immunohistochemistry and immunoblotting. Results: Compared with PD group, the proportion of striatum-penetrating synapses in PD exercise group was significantly lower than that in PD group (P <0.05). Glu concentration in striatum in PD exercise group was significantly lower than that in PD group (P <0.01). The expression of D2DR and NMDAR1 in striatum in PD exercise group was significantly increased compared with PD group (P <0.05, P <0.05). Conclusion: Exercise intervention improves the neurotransmission of cortical-striatum neurons in PD model rats, which may be related to the enhancement of synaptic activity of Glu by DA.