Wang Zhi-Yong, Lian Hui, Cai Qing-Qing, Song Hai-Yan, Zhang Xiao-Li, Zhou Li, Zhang Yi-Min, Zheng Li-Fei, Zhu Jin-Xia
Key Laboratory for Medical Tissue Regeneration of Henan Province, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China.
Key Laboratory for Medical Tissue Regeneration of Henan Province, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, China Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
J Parkinsons Dis. 2014;4(3):375-83. doi: 10.3233/JPD-130279.
Parkinson's disease (PD) is a neurodegenerative disorder that is characterized by degeneration of dopaminergic neurons in the substantia nigra (SN). Destruction of the SN can lead to gastric dyskinesis accompanied by decreased expression of choline acetyltransferase (ChAT) and increased expression of tyrosine hydroxylase (TH) in the dorsal vagus complex (DVC), which includes the dorsal motor nucleus of the vagus (DMV) and nucleus tractus solitarius (NTS). However, it is unclear if the SN and DVC are directly connected.
To investigate the neural projection from the SN to the DVC in rats.
Retrograde and anterograde tracing techniques combined with double-labeling immunofluorescence technique were used.
Destruction of the SN significantly decreases ChAT immunoreactivity (IR) and increases TH-IR in the DVC. After injection of the retrograde tracer fluoro-gold (FG) into the DVC, FG-labeled neurons were observed in the hypothalamic paraventricular nucleus (PVN), lateral hypothalamus (LH), inferior olive (IO), and locus coeruleus (LC). No FG-positive cells were observed in the SN or striatum. Furthermore, after injection of anterograde tracer biotinylated dextran amine (BDA) into the SN, BDA-positive fibers were observed in the caudate putamen (Cpu), globus pallidus (GP), LC, and LH but not in the DVC.
This study is the first to demonstrate that neurons in the SN do not directly innervate the DVC in rats. The DVC might be indirectly innervated by the SN through the hypothalamus and/or the LC. These data provide important morphological insights into the potential mechanism underlying the gastroparesis observed in PD patients.
帕金森病（PD）是一种神经退行性疾病，其特征是黑质（SN）中多巴胺能神经元变性。SN的破坏可导致胃运动障碍，伴有迷走神经背核复合体（DVC）中胆碱乙酰转移酶（ChAT）表达降低和酪氨酸羟化酶（TH）表达增加，DVC包括迷走神经背运动核（DMV）和孤束核（NTS）。然而，SN和DVC是否直接相连尚不清楚。
研究大鼠中从SN到DVC的神经投射。
采用逆行和顺行示踪技术结合双标免疫荧光技术。
SN破坏显著降低DVC中的ChAT免疫反应性（IR）并增加TH-IR。将逆行示踪剂氟金（FG）注入DVC后，在下丘脑室旁核（PVN）、下丘脑外侧区（LH）、下橄榄核（IO）和蓝斑（LC）中观察到FG标记的神经元。在SN或纹状体中未观察到FG阳性细胞。此外，将顺行示踪剂生物素化葡聚糖胺（BDA）注入SN后，在尾壳核（Cpu）、苍白球（GP）、LC和LH中观察到BDA阳性纤维，但在DVC中未观察到。
本研究首次证明大鼠SN中的神经元不直接支配DVC。DVC可能通过下丘脑和/或LC由SN间接支配。这些数据为PD患者中观察到的胃轻瘫的潜在机制提供了重要的形态学见解。
