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LPS 诱导 PD 大鼠模型中 DMV 中 TH 和 ChAT 免疫反应性神经元的改变和胃动力障碍。

Alterations in TH- and ChAT-immunoreactive neurons in the DMV and gastric dysmotility in an LPS-induced PD rat model.

机构信息

Key Laboratory for Medical Tissue Regeneration of Henan Province, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, China; Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.

出版信息

Auton Neurosci. 2013 Oct;177(2):194-8. doi: 10.1016/j.autneu.2013.04.012. Epub 2013 May 20.

DOI:10.1016/j.autneu.2013.04.012
PMID:23701914
Abstract

To study movement disorder in Parkinson's disease (PD), an animal model of PD can be created by injecting lipopolysaccharide (LPS) into the substantia nigra of rats. In addition to body movement disorders, patients with PD often experience gastrointestinal (GI) dysfunction, such as gastroparesis. However, the underlying mechanism of these disorders remains unclear. The dorsal motor nucleus of vagus (DMV) is a well-known visceral nucleus that regulates GI function. The present study investigated alterations in DMV neurons and gastric motility in rats with LPS-induced PD (LPS-PD rats). Gastric motility was recorded using a strain gauge force transducer in vivo. The distributions of tyrosine hydroxylase (TH)- and choline acetyltransferase (ChAT)-positive neurons in the DMV were determined using immunofluorescence and confocal laser microscopy. Our results indicated that in LPS-PD rats, the number of neurons in the substantia nigra, including neurons with TH immunoreactivity, was markedly reduced, although glial cell proliferation was clearly observed. However, enhanced TH immunoreactivity and decreased ChAT immunoreactivity were found in the DMV. Furthermore, weakened gastric motility was recorded in anesthetized LPS-PD rats. In conclusion, rats with LPS-induced PD exhibited gastric dysmotility with an alteration in DMV neurons. This PD model may be used to study autonomic nervous system disorders that are often observed in patients with early-stage PD.

摘要

为了研究帕金森病(PD)中的运动障碍,可以通过向大鼠黑质内注射脂多糖(LPS)来创建 PD 的动物模型。除了身体运动障碍外,PD 患者还经常出现胃肠道(GI)功能障碍,如胃轻瘫。然而,这些疾病的潜在机制仍不清楚。迷走神经背核(DMV)是一个众所周知的内脏核,调节 GI 功能。本研究探讨了 LPS 诱导的 PD(LPS-PD 大鼠)大鼠 DMV 神经元和胃动力的变化。使用应变计力换能器在体内记录胃动力。使用免疫荧光和共聚焦激光显微镜确定 DMV 中酪氨酸羟化酶(TH)和胆碱乙酰转移酶(ChAT)阳性神经元的分布。我们的结果表明,在 LPS-PD 大鼠中,包括具有 TH 免疫反应性的神经元在内的黑质内神经元数量明显减少,尽管明显观察到神经胶质细胞增殖。然而,在 DMV 中发现 TH 免疫反应性增强和 ChAT 免疫反应性降低。此外,在麻醉的 LPS-PD 大鼠中记录到胃动力减弱。总之,LPS 诱导的 PD 大鼠表现出胃动力障碍,DMV 神经元发生改变。这种 PD 模型可用于研究常发生在早期 PD 患者中的自主神经系统障碍。

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