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A5 去甲肾上腺素能神经元与新生大鼠的呼吸控制。

A5 noradrenergic neurons and breathing control in neonate rats.

机构信息

Department of Morphology and Animal Physiology - FCAV, São Paulo State University (UNESP), Via de acesso Paulo Donato Castellane s/n, Jaboticabal, SP, 14870-900, Brazil.

Department of Pediatrics, Centre de Recherche de L'Institut Universitaire de Cardiologie Et de Pneumologie de Québec, Université Laval, Québec, G1V 4G5, Canada.

出版信息

Pflugers Arch. 2021 Jun;473(6):859-872. doi: 10.1007/s00424-021-02550-1. Epub 2021 Apr 14.

Abstract

The pontine A5 noradrenergic group contributes to the maturation of the respiratory system before birth in rats. These neurons are connected to the neural network responsible for respiratory rhythmogenesis. In the present study, we investigated the participation of A5 noradrenergic neurons in neonates (P7-8 and P14-15) in the control of ventilation during hypoxia and hypercapnia in in vivo experiments using conjugated saporin anti-dopamine beta-hydroxylase (DβH-SAP) to specifically ablate noradrenergic neurons. Thus, DβH-SAP (420 ng/μL) or saporin (SAP, control) was injected into the A5 region of neonatal male Wistar rats. Hypoxia reduced respiratory variability in control animals; however, A5 lesion prevented this effect in P7-8 rats. Our data suggest that noradrenergic neurons of the A5 region in neonate rats do not participate in the control of ventilation under baseline and hypercapnic conditions, but exert an inhibitory modulation on breathing variability under hypoxic challenge in early life (P7-8).

摘要

脑桥 A5 去甲肾上腺素能神经元群有助于大鼠出生前呼吸系统的成熟。这些神经元与负责呼吸节律发生的神经网络相连。在本研究中,我们使用共轭型 SAP 抗多巴胺β羟化酶(DβH-SAP)特异性地破坏去甲肾上腺素能神经元,在体内实验中研究了 A5 去甲肾上腺素能神经元在新生儿(P7-8 和 P14-15)中对缺氧和高碳酸血症期间通气控制的参与。因此,将 DβH-SAP(420ng/μL)或 SAP(对照)注入新生雄性 Wistar 大鼠的 A5 区域。在对照动物中,缺氧降低了呼吸变异性;然而,A5 损伤阻止了 P7-8 大鼠的这种作用。我们的数据表明,新生大鼠 A5 区的去甲肾上腺素能神经元在基础和高碳酸血症条件下不参与通气控制,但在早期生命(P7-8)的缺氧挑战下对呼吸变异性发挥抑制性调制作用。

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