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水下潜水对大鼠脑干神经元的激活作用。

Activation of brainstem neurons by underwater diving in the rat.

作者信息

Panneton W Michael, Gan Qi, Le Jason, Livergood Robert S, Clerc Philip, Juric Rajko

机构信息

Department of Pharmacological and Physiological Science, St. Louis University School of Medicine St. Louis, MO, USA.

出版信息

Front Physiol. 2012 May 3;3:111. doi: 10.3389/fphys.2012.00111. eCollection 2012.

DOI:10.3389/fphys.2012.00111
PMID:22563319
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3342523/
Abstract

The mammalian diving response is a powerful autonomic adjustment to underwater submersion greatly affecting heart rate, arterial blood pressure, and ventilation. The bradycardia is mediated by the parasympathetic nervous system, arterial blood pressure is mediated via the sympathetic system and still other circuits mediate the respiratory changes. In the present study we investigate the cardiorespiratory responses and the brainstem neurons activated by voluntary diving of trained rats, and, compare them to control and swimming animals which did not dive. We show that the bradycardia and increase in arterial blood pressure induced by diving were significantly different than that induced by swimming. Neuronal activation was calculated after immunohistochemical processing of brainstem sections for Fos protein. Labeled neurons were counted in the caudal pressor area, the medullary dorsal horn, subnuclei of the nucleus tractus solitarii (NTS), the nucleus raphe pallidus (RPa), the rostroventrolateral medulla, the A5 area, the nucleus locus coeruleus, the Kölliker-Fuse area, and the external lateral and superior lateral subnuclei of the parabrachial nucleus. All these areas showed significant increases in Fos labeling when data from voluntary diving rats were compared to control rats and all but the commissural subnucleus of the NTS, A5 area, and RPa were significantly different from swimming rats. These data provide a substrate for more precise experiments to determine the role of these nuclei in the reflex circuits driving the diving response.

摘要

哺乳动物的潜水反应是对水下浸没的一种强大的自主调节,对心率、动脉血压和通气有很大影响。心动过缓由副交感神经系统介导,动脉血压由交感神经系统介导,还有其他回路介导呼吸变化。在本研究中,我们调查了训练有素的大鼠自愿潜水所激活的心肺反应和脑干神经元,并将它们与未潜水的对照动物和游泳动物进行比较。我们发现,潜水诱导的心动过缓和动脉血压升高与游泳诱导的有显著差异。在对脑干切片进行Fos蛋白免疫组织化学处理后计算神经元激活情况。在尾侧加压区、延髓背角、孤束核(NTS)亚核、中缝苍白核(RPa)、延髓头端腹外侧、A5区、蓝斑核、柯利克-福斯区以及臂旁核的外侧和上外侧亚核中计数标记神经元。当将自愿潜水大鼠的数据与对照大鼠的数据进行比较时,所有这些区域的Fos标记均显著增加,除了NTS的连合亚核、A5区和RPa外,所有区域与游泳大鼠相比均有显著差异。这些数据为更精确的实验提供了基础,以确定这些核团在驱动潜水反应的反射回路中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/54e97f2e7386/fphys-03-00111-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/b6886373543e/fphys-03-00111-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/c8f389b171ae/fphys-03-00111-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/eb7845358910/fphys-03-00111-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/a6959a98084e/fphys-03-00111-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/a4c2f10ed032/fphys-03-00111-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/54e97f2e7386/fphys-03-00111-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/b6886373543e/fphys-03-00111-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/c8f389b171ae/fphys-03-00111-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/eb7845358910/fphys-03-00111-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/01b11850bece/fphys-03-00111-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/a6959a98084e/fphys-03-00111-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/a4c2f10ed032/fphys-03-00111-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d43/3342523/54e97f2e7386/fphys-03-00111-g007.jpg

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