中文摘要：

目的：观察尼古丁对多巴胺能神经元的作用并探讨其作用机制。方法：采用1-甲基-4-苯基-1，2，3,6-四氢吡啶（1-methyl-4-phenyl—1，2，3，6-tetrahydmpyridine，MPTP）小鼠模型，通过行为学方法、免疫组织化学、电镜观察尼古丁预处理对帕金森病（parkinson’s disease，PD）小鼠的影响。结果：尼古丁预处理可以明显缩短PD小鼠的爬杆时间，提高悬挂的得分。免疫组化结果显示尼古丁显著减少多巴胺（doparnine，DA）能神经元变性（P〈0．01）和γ-氨基丁酸（γ-aminobutyric acid，GABA）能神经元的脱失（P〈0．05），并可减轻尾核超微结构的损伤。结论：尼古丁可减轻MPTP小鼠多巴胺能神经元的损伤，对多巴胺能神经元有保护作用。

英文摘要：

To investigate the protective effect of nicotine on dopaminergic neurons and its mechanisms in mice with parkinson＇s disease（PD） induced by 1-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine（ MPTP）. Methods： C57BL/6J mice were injected with MPTP for 8 days to establish PD model. Nicotine was given for 10 days in the pretreatment group. Animals were examined behaviorally with the pole test and traction test. Tyrosine hydroxylase（TH） and γ-aminobutyric acid（GABA） were investigated by the immunocytoche- mistry（ICC） method. The uhrastructural changes of caudate nucleus（CN） were observed by electron microscope. Results： The resuits showed that pretreatment nicotine could improve the dyskinesia of PD mice markedly. Simultaneously, TH（ P 〈 0.01 ） neurons and GABA（P〈0.05） neurons were much more in the pretreatment group when compared with those in the model group. The ultrastructural injury of the pretreatment group was also ameliorated. Conclusion： Nicotine has a protective effect on the dopaminergic neurons in the MPTP-treated mice.