Loss of nigrostriatal dopamine (DA) in Parkinson's disease results in over‐activation/bursting of the subthalamic nucleus (STN). The STN projects to the substantia nigra (SN) pars compacta (SNpc) and pars reticulata (SNpr). The vesicular glutamate transporter 2 (Vglut2) is localized within at least STN terminals synapsing within the SN, but it is not known if there are differential changes in the Vglut2+ input to the SNpc versus SNpr following DA loss. The goal/rationale of this current study was to determine whether there were differential changes in the density/levels of glutamate immuno‐gold labeling within Vglut2+ nerve terminals synapsing in the SNpc/SNpr and in the proportion of Vglut2+ terminals contacting tyrosine hydroxylase (TH) positively(+) or negatively(−) labeled dendrites following DA loss. Within the SNpc, there was a significant increase (51.3%) in the density of nerve terminal glutamate immuno‐gold labeling within Vglut2+ terminals synapsing on TH(−) dendrites following MPTP versus the vehicle (VEH) group. There was a significant decrease (16%) in the percentage of Vglut2+ terminals contacting TH(+) labeled dendrites in the MPTP‐ versus VEH‐treated group within the SNpc. Within the SNpr, there was a significant decrease in the density of glutamate immuno‐gold labeling in Vglut2+ terminals contacting TH(+) (71.5%) and TH(−) (55.5%) labeled dendrites, suggesting an increase in glutamate release. There was no change in the percentage of Vglut2+ terminals contacting TH(+) or TH(−) dendrites in the SNpr. We conclude that there is a differential effect following DA loss on the glutamate input from Vglut2+ terminals synapsing within the SNpr versus SNpc.

中文翻译：

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在帕金森氏病进行性小鼠模型中，黑质纹状体多巴胺流失后，黑质致密部/网状组织的Vglut2谷氨酸能输入的差异性超微结构改变

帕金森氏病中黑质纹状体多巴胺（DA）的丢失会导致丘脑下核（STN）过度活化/破裂。STN投影到黑质（SN）致密粉（SNpc）和网状（SNpr）。囊泡谷氨酸转运蛋白2（Vglut2）至少位于SN内突触的STN末端，但尚不清楚DA丢失后SNpc与SNpr的Vglut2 +输入是否存在差异。这项当前研究的目的/理由是确定在SNpc / SNpr突触的Vglut2 +神经末梢内谷氨酸免疫金标记的密度/水平和接触酪氨酸羟化酶（TH）的Vglut2 +末梢比例是否存在差异DA丧失后，标记为正（+）或标记为负（-）的树突。在SNpc中，VEH）组。在SNpc中，MPTP处理组和VEH处理组中，接触TH（+）标记树突的Vglut2 +末端百分比显着降低（16％）。在SNpr中，接触TH（+）（71.5％）和TH（-）（55.5％）标记的树突的Vglut2 +末端的谷氨酸免疫金标记密度显着降低，表明谷氨酸释放增加。SNpr中接触TH（+）或TH（-）树突的Vglut2 +末端的百分比没有变化。我们得出的结论是，DA损失对SNpr与SNpc内突触的Vglut2 +末端的谷氨酸输入有不同的影响。