Aymerich M S, Barroso-Chinea P, Pérez-Manso M, Muñoz-Patiño A M, Moreno-Igoa M, González-Hernández T, Lanciego J L
Neuromorphology-Tracing Laboratory, Department of Neurosciences, Center for Applied Medical Research, University of Navarra Medical College, Pio XII Avenue no. 55, 31008 Pamplona, Spain.
Eur J Neurosci. 2006 Apr;23(8):2099-108. doi: 10.1111/j.1460-9568.2006.04741.x.
The position of the caudal intralaminar nuclei within basal ganglia circuitry has largely been neglected in most studies dealing with basal ganglia function. During the past few years, there has been a growing body of evidence suggesting that the thalamic parafascicular nucleus in rodents (PF) exerts a multifaceted modulation of basal ganglia nuclei, at different levels. Our aim was to study the activity of the thalamostriatal pathway in rats with unilateral dopaminergic depletion. The experimental approach comprised first unilateral delivery of 6-OHDA in the medial forebrain bundle. Thirty days post-lesioning, animals showing a clear asymmetry were then subjected to bilateral injection of Fluoro-Gold (FG) within the striatum. Subsequently, expression of the mRNA encoding the vesicular glutamate transporter 2 (vGLUT2) was detected within thalamostriatal-projecting neurons (FG-labeled) by in situ hybridization and the results were confirmed by laser-guided capture microdissection microscopy followed by real-time PCR. The data showed that there was a marked neuronal loss restricted to PF neurons projecting to the dopamine-depleted striatum. Moreover, PF neurons innervating the dopamine-depleted striatum were intensely hyperactive. These neurons showed a marked increase on the expression of vGLUT2 mRNA as well as for the mRNA encoding the subunit I of cytochrome oxidase as compared with those neurons projecting to the striatum with normal dopamine content. Thus, the selective neurodegeneration of PF neurons innervating the striatum together with the increased activity of the thalamostriatal pathway coexist after nigrostriatal denervation.
在大多数关于基底神经节功能的研究中，尾侧板内核在基底神经节神经回路中的位置在很大程度上被忽视了。在过去几年中，越来越多的证据表明，啮齿动物的丘脑束旁核（PF）在不同水平上对基底神经节核团发挥多方面的调节作用。我们的目的是研究单侧多巴胺能耗竭大鼠丘脑纹状体通路的活动。实验方法首先是在内侧前脑束单侧注射6-羟基多巴胺。损伤后30天，对表现出明显不对称的动物在纹状体内进行双侧注射荧光金（FG）。随后，通过原位杂交检测丘脑纹状体投射神经元（FG标记）中编码囊泡谷氨酸转运体2（vGLUT2）的mRNA表达，并通过激光引导捕获显微切割显微镜检查和实时PCR对结果进行确认。数据显示，投射到多巴胺耗竭纹状体的PF神经元存在明显的神经元丢失。此外，支配多巴胺耗竭纹状体的PF神经元高度活跃。与投射到多巴胺含量正常的纹状体的神经元相比，这些神经元的vGLUT2 mRNA以及编码细胞色素氧化酶亚基I的mRNA表达显著增加。因此，黑质纹状体去神经支配后，支配纹状体的PF神经元选择性神经变性与丘脑纹状体通路活性增加并存。
