单胺能神经元,化学感觉和觉醒

M.A. Haxhiu , F. Tolentino-Silva , G. Pete , P. Kc , S.O. Mack
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引用次数: 81

摘要

近年来,在细胞和功能水平上对中枢化学敏感性的理解取得了巨大进展。结合分子生物学技术(早期基因表达作为细胞活化的指标)和神经递质免疫组织化学,产生了与化学感觉细胞中神经化学编码相关的新信息。我们发现,二氧化碳暴露导致沿神经轴的离散细胞群的激活,包括属于单胺能细胞、去甲肾上腺素、血清素和含组胺神经元的细胞亚群。在某种程度上,它们可能在高碳酸血症的呼吸反应中发挥调节作用,这可能与它们的行为状态控制功能有关。增加CO2/H+激活单胺能神经元可促进呼吸相关运动放电,特别是上呼吸道扩张肌的活动。此外,这些神经元协调交感神经和副交感神经对内脏器官的张力,并参与调节血流与运动活动水平。由相互关联的单胺能核组成的网络的二氧化碳化学敏感性的任何缺陷都可能导致运动输出的障碍,神经内分泌和对睡眠中危及生命的挑战(如窒息)的稳态反应的失败。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Monoaminergic neurons, chemosensation and arousal

In recent years, immense progress has been made in understanding central chemosensitivity at the cellular and functional levels. Combining molecular biological techniques (early gene expression as an index of cell activation) with neurotransmitter immunohistochemistry, new information has been generated related to neurochemical coding in chemosensory cells. We found that CO2 exposure leads to activation of discrete cell groups along the neuraxis, including subsets of cells belonging to monoaminergic cells, noradrenaline-, serotonin-, and histamine-containing neurons. In part, they may play a modulatory role in the respiratory response to hypercapnia that could be related to their behavioral state control function. Activation of monoaminergic neurons by an increase in CO2/H+ could facilitate respiratory related motor discharge, particularly activity of upper airway dilating muscles. In addition, these neurons coordinate sympathetic and parasympathetic tone to visceral organs, and participate in adjustments of blood flow with the level of motor activity. Any deficit in CO2 chemosensitivity of a network composed of inter-related monoaminergic nuclei might lead to disfacilitation of motor outputs and to failure of neuroendocrine and homeostatic responses to life-threatening challenges (e.g. asphyxia) during sleep.

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