电针促进帕金森小鼠多巴胺神经元突触可塑性的细胞分子机制

【作者】 唐勇；

【导师】 黄迪君；

【作者基本信息】 成都中医药大学 ， 针灸推拿， 2004， 博士

【摘要】 目的：研究电针对帕金森小鼠黑质致密部多巴胺神经元突触可塑性的影响及细胞分子机制。方法：以1—甲基—4苯基—1，2，3，6四氢吡啶诱导的帕金森小鼠作为研究对象，电针“合谷”、“太冲”穴，每日1次，7次为1疗程，共3个疗程后，尼氏染色检测黑质致密部神经元变性情况；电镜检测黑质致密部突触形态变化；免疫组化检测酪氨酸羟化酶、脑源性神经营养因子、神经细胞粘附分子、多巴胺转运体、巢蛋白表达；原位杂交检测酪氨酸羟化酶、脑源性神经营养因子、神经细胞粘附分子、多巴胺转运体mRNA表达。结果：模型组小鼠尼氏染色阳性细胞计数减少，电针后增多；电针后黑质致密部突触数目增多、数密度、面密度增大；电针后帕金森小鼠与模型组比较，酪氨酸羟化酶、脑源性神经营养因子、神经细胞粘附分子、多巴胺转运体、巢蛋白表达增强；电针后酪氨酸羟化酶、脑源性神经营养因子、神经细胞粘附分子、多巴胺转运体mRNA表达也增强。结论：电针促进帕金森小鼠多巴胺神经元突触可塑性的细胞分子基础可能与脑源性神经营养因子的神经营养作用、神经细胞粘附分子的细胞粘附、对内源性神经干细胞的原位诱导和促进多巴胺的合成与重摄取有关。更多还原

【Abstract】 Objective: To research on doparainegic neuron synapse plasticity and its celluar molecular mechanism of substantia nigra in Parkinson’ s disease model mouse treated by electroacupuncture therapy. Methods:The parkinson’ s disease mouce induced by 1-methyl, 4-phenyl - 1, 2,3,6 tetrahydropyridine were treated by electroacupuncture therapy on "Hegu(LI4)" and "Taichong(LVS)" acupoints. The treatment was once daily and up to seven as one course which was lasted for 3 courses. Nissles stain for detecting dopaminergic nuron degeneration; electron microscope detecting for morphylogical changes of the dopaminegic neuron synapse plasticity in substantial nigra zone compacta; Immunohistochemistry for the exppresion of tyrosine hydroxylase, brain-derived neurotrophic factor, neural cell adhesion molecules, dopamine transpotor, nestin; in situ hybridization histochemistry was applied for testing expresion of tyrosine hydroxylase, brain-derived neurotrophic factor, neural cell adhesion molecules and dopaminetranspotor mRNA. Results: The positive cell numbers of nissles stainin model mouce increased after electroacupuncture; The decreased dopaminergic nuron synapses in model mouse were increased in substantial nigra after acunpuncture treatment in which the number density and volume density also enlarged; Compared to model mouse, the expressions of tyrosine hydroxylase, brain-derived neurotrophic factor, neural cell adhesion molecules, dopamine transpotor, nestin were enhaced; the mRNA exression of tyrosine hydroxylase, brain-derived neurotrophic factor,neural cell adhesion molecules and dopamine transpotor enhaced, too. Conclusions: Electroacupuncture therapy can promote the synapticplasticity of the degenerative dopaminergic neuron in parkinson’ s disease mouse. The celluar molecular mechanism is related to the effective of neuronal nourishment by brain-derived neurotrophic factor, cell adhension of neural cell adhesion molecules, endogenous induction of nerve stem cell and acceleration of the synethis and metabolism of dopamine.更多还原