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。
Aim: This study aimed at observing the effects of exercise on synapses ultrastructure of striatum,glutamatergic( Glu) concentration and expressions of D2 DR and NMDAR1 in Parkinson( PD) rats,and investigating the mechanism of exercise regulating Glu neurotransmission of cortex striatum in PD rats. Methods: Male SD rats were randomly divided into Control group,Control + Ex group,PD group and PD + Ex group,18 rats in each group. PD rats were established by injection of 6- OHDA in medial forebrain bundle single point while Control and Control + Ex groups rats received the same dose of saline. Exercise group rats participated in 4 weeks exercise,exercise program is 11 m / min,30 min / day,and 5 days / week. The synaptic ultrastructure of cortex-striatum was observed by transmission electron microscope( TEM),Glu level in striatum was detected by high performance liquid chromatography( HPLC),the striatal D2 DR and NMDAR1 expressions were tested by Immunohistochemistry and Western blotting. Results: Compared with PD group,the proportion of striatal perforated synapses and the Glu concentration in PD + Ex group were significantly lower( P〈 0. 05,P 〈0. 01),striatal D2 DR and NMDAR1 expressions in PD + Ex group were significantly higher( Ps〈 0. 05). Conclusion: Exercise improves corted-striatum Glu neurotransmission in PD rats,which may be related to the improved effect of dopamine regulating cortex striatum Glu neurotransmission.