暴露于缺氧、高碳酸血症或高碳酸血症的大鼠 A1/C1 神经元中的 Fos 表达。

IF 2.5 4区 医学 Q3 NEUROSCIENCES
Kouki Kato , Risa Serizawa , Takuya Yokoyama , Nobuaki Nakamuta , Yoshio Yamamoto
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引用次数: 0

摘要

比较了暴露于缺氧(10 % O2)、高碳酸血症(8 % CO2)和高碳酸血症缺氧(8 % CO2和10 % O2)2小时的大鼠腹外侧延髓儿茶酚胺能神经元中具有多巴胺β-羟化酶(DBH)免疫反应的Fos表达分布情况。在各实验组中,缺氧暴露组大鼠腹外侧延髓喙区的 Fos/DBH 双免疫反应神经元数量多于对照组(20 % O2),特别是在距面神经核尾端 + 150 μm 至 + 2,400 μm 的范围内。另一方面,在高碳酸血症暴露大鼠的腹外侧延髓区域几乎没有观察到 Fos/DBH 双免疫反应神经元。高碳酸缺氧暴露大鼠的双免疫反应神经元数量与对照组相当。本研究结果表明,肾上腺素能 C1 神经元被缺氧特异性激活,并参与呼吸和循环功能的调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Fos expression in A1/C1 neurons of rats exposed to hypoxia, hypercapnia, or hypercapnic hypoxia
The distribution of Fos expression in catecholaminergic neurons with immunoreactivity for dopamine β-hydroxylase (DBH) of the ventrolateral medulla was compared between rats exposed to hypoxia (10 % O2), hypercapnia (8 % CO2), and hypercapnic hypoxia (8 % CO2 and 10 % O2) for 2 h. Among the experimental groups, hypoxia-exposed rats had more Fos/DBH double-immunoreactive neurons than the control group (20 % O2) in the rostral area of the ventrolateral medulla, specifically in the range of + 150 μm to + 2,400 μm from the caudal end of the facial nerve nucleus. On the other hand, Fos/DBH double-immunoreactive neurons were scarcely observed in the ventrolateral medullary region of hypercapnia-exposed rats. The number of double-immunoreactive neurons in hypercapnic hypoxia-exposed rats was comparable to that in the control group. The present results suggest that adrenergic C1 neurons are specifically activated by hypoxia and are involved in the regulation of respiratory and circulatory functions.
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来源期刊
Neuroscience Letters
Neuroscience Letters 医学-神经科学
CiteScore
5.20
自引率
0.00%
发文量
408
审稿时长
50 days
期刊介绍: Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.
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