Striatal-direct and -indirect Pathway Neurons showed different vulnerability in basal ganglia disorders. Therefore, present study aimed to examine and compare characteristic changes of densities, protein and mRNA levels of soma, dendrites, and spines between striatal-direct and -indirect pathway neurons after DA depletion by using immunohistochemistry, Western blotting, real-time PCR and immunoelectron microscopy techniques. Experimental results showed that: 1) 6OHDA-induced DA depletion decreased the soma density of striatal-direct pathway neurons (SP+), but no significant changes for striatal-indirect pathway neurons (ENK+). 2) DA depletion resulted in a decline of dendrite density for both striatal-direct (D1+) and -indirect (D2+) pathway neurons, and D2+ dendritic density declined more obviously. At the ultrastructure level, the densities of D1+ and D2+ dendritic spines reduced in the 6OHDA groups compared with their control groups, but the density of D2+ dendritic spines reduced more significant than that of D1. 3) Striatal DA depletion down-regulated protein and mRNA expression levels of SP and D1, on the contrary, ENK and D2 protein and mRNA levels of indirect pathway neurons were up-regulated significantly. Present results suggested that indirect pathway neurons be more sensitive to 6OHDA-induced DA depletion.

纹状体直接和间接途径神经元在基底神经节疾病中显示出不同的脆弱性。因此，本研究旨在通过免疫组织化学，Western印迹，实时荧光定量PCR和免疫电子方法检查和比较DA耗竭后纹状体直接和间接途径神经元之间的体细胞，树突和棘突的密度，蛋白质和mRNA水平的特征变化。显微镜技术。实验结果表明：1）6OHDA诱导的DA耗竭降低了纹状体直接途径神经元（SP +）的体细胞密度，但对于纹状体间接途径神经元（ENK +）则无明显变化。2）DA耗竭导致纹状体直接（D1 +）和-间接（D2 +）通路神经元的树突密度下降，而D2 +树突密度下降更为明显。在超微结构层面，与对照组相比，6OHDA组中D1 +和D2 +树突棘的密度降低，但是D2 +树突棘的密度比D1显着降低。3）纹状体DA消耗下调SP和D1的蛋白质和mRNA表达水平，相反，间接途径神经元的ENK和D2蛋白质和mRNA表达显着上调。目前的结果表明，间接途径神经元对6OHDA诱导的DA耗竭更为敏感。间接途径神经元的ENK和D2蛋白和mRNA水平显着上调。目前的结果表明，间接途径神经元对6OHDA诱导的DA耗竭更为敏感。间接途径神经元的ENK和D2蛋白和mRNA水平显着上调。目前的结果表明，间接途径神经元对6OHDA诱导的DA耗竭更为敏感。