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单侧迷走神经切断术对大鼠迷走神经背侧复合体中一氧化氮合酶和组胺H3受体的影响。

Effects of unilateral vagotomy on nitric oxide synthase and histamine H3 receptors in the rat dorsal vagal complex.

作者信息

Zhao X L, Yanai K, Hashimoto Y, Steinbusch H W, Watanabe T

机构信息

Department of Pharmacology I, Tohoku University School of Medicine, Sendai, Japan.

出版信息

J Chem Neuroanat. 1996 Oct;11(4):221-9. doi: 10.1016/s0891-0618(96)00163-9.

DOI:10.1016/s0891-0618(96)00163-9
PMID:8951592
Abstract

Nitric oxide synthase (NOS) and histamine H3 receptors are both markedly increased by neuronal injuries. To examine whether peripheral axotomy produced differential changes in NOS and H3 receptors, both NOS and H3 receptors were measured in the dorsal vagal complex after unilateral vagotomy. The presence of NOS-positive neurons was examined using both NADPH-diaphorase histochemistry and neuronal NOS-immunohistochemistry in rats vagotomized at the mid-cervical level. NADPH-diaphorase activity and NOS-immunoreactivity were markedly enhanced on the dorsal motor nucleus of the vagus (DMX) and in the ambiguous nucleus at the denervated side. Intraperitoneal injection of NOS inhibitors, N omega-nitro-L-arginine (10 mg/kg) or dexamethasone (0.5 mg/kg) attenuated the increase in NADPH-diaphorase activity. Glial fibrillary acidic protein (GFAP) was similarly induced 2 weeks after vagotomy in the vagal complex and surrounding area. Histamine H3 receptors in the vagal complex were visualized with [3H]N alpha-methylhistamine. The ligand-labeled H3 receptors were mainly located at the nucleus of the solitary tract (NST). The densities of H3 receptors did not change in the NST after unilateral vagotomy. These results suggest that peripheral axotomy such as mid-cervical vagotomy preferentially induces NOS in damaged neurons without affecting the level of H3 receptors.

摘要

一氧化氮合酶(NOS)和组胺H3受体在神经元损伤后均显著增加。为了研究外周轴突切断术是否会使NOS和H3受体产生不同变化,在单侧迷走神经切断术后,对迷走神经背侧复合体中的NOS和H3受体进行了检测。使用NADPH黄递酶组织化学和神经元型NOS免疫组织化学方法,对颈中部切断迷走神经的大鼠迷走神经背侧运动核(DMX)和疑核中NOS阳性神经元的存在情况进行了检查。在去神经侧的DMX和疑核中,NADPH黄递酶活性和NOS免疫反应性显著增强。腹腔注射NOS抑制剂Nω-硝基-L-精氨酸(10mg/kg)或地塞米松(0.5mg/kg)可减弱NADPH黄递酶活性的增加。迷走神经切断术后2周,迷走神经复合体及其周围区域同样诱导了胶质纤维酸性蛋白(GFAP)的表达。用[3H]Nα-甲基组胺显示迷走神经复合体中的组胺H3受体。配体标记的H3受体主要位于孤束核(NST)。单侧迷走神经切断术后,NST中H3受体的密度没有变化。这些结果表明,外周轴突切断术,如颈中部迷走神经切断术,优先诱导受损神经元中的NOS,而不影响H3受体的水平。

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