Taxini Camila L, Moreira Thiago S, Takakura Ana C, Bícego Kênia C, Gargaglioni Luciane H, Zoccal Daniel B
Department of Morphology and Animal Physiology, São Paulo State University (UNESP), Jaboticabal, SP, Brazil.
Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo (USP), São Paulo, SP, Brazil.
Neuroscience. 2017 Jun 23;354:146-157. doi: 10.1016/j.neuroscience.2017.04.033. Epub 2017 Apr 29.
The A5 area at the ventrolateral pons contains noradrenergic neurons connected with other medullary areas involved in the cardiorespiratory control. Its contribution to the cardiorespiratory regulation was previously evidenced in anesthetized conditions. In the present study, we investigated the involvement of the A5 noradrenergic neurons to the basal and chemoreflex control of the sympathetic and respiratory activities in unanesthetized conditions. A5 noradrenergic neurons were lesioned using microinjections of anti-dopamine β-hydroxylase saporin (anti-DβH-SAP). After 7-8days, we evaluated the arterial pressure levels, heart rate and minute ventilation in freely moving adult rats (280-350g) as well as recorded from thoracic sympathetic (tSN) and phrenic nerves (PN) using the arterially perfused in situ preparation of juvenile rats (80-90g). Baseline cardiovascular, sympathetic and respiratory parameters were similar between control (n=7-8) and A5-lesioned rats (n=5-6) in both experimental preparations. In adult rats, lesions of A5 noradrenergic neurons did not modify the reflex cardiorespiratory adjustments to hypoxia (7% O) and hypercapnia (7% CO). In the in situ preparations, the sympatho-excitation, but not the PN reflex response, elicited by either the stimulation of peripheral chemoreceptors (ΔtSN: 110±12% vs 58±8%, P<0.01) or hypercapnia (ΔtSN: 9.5±1.4% vs 3.9±1.7%, P<0.05) was attenuated in A5-lesioned rats compared to controls. Our data demonstrated that A5 noradrenergic neurons are part of the circuitry recruited for the processing of sympathetic response to hypoxia and hypercapnia in unanesthetized conditions.
脑桥腹外侧的A5区域含有去甲肾上腺素能神经元,这些神经元与参与心肺控制的其他延髓区域相连。其对心肺调节的作用先前已在麻醉状态下得到证实。在本研究中,我们调查了A5去甲肾上腺素能神经元在未麻醉状态下对交感神经和呼吸活动的基础及化学反射控制中的作用。使用抗多巴胺β-羟化酶皂草素(anti-DβH-SAP)微量注射损毁A5去甲肾上腺素能神经元。7-8天后,我们评估了自由活动的成年大鼠(280-350克)的动脉压水平、心率和分钟通气量,并使用幼年大鼠(80-90克)的动脉灌注原位标本记录胸段交感神经(tSN)和膈神经(PN)的活动。在两种实验标本中,对照大鼠(n=7-8)和A5损毁大鼠(n=5-6)的基线心血管、交感神经和呼吸参数相似。在成年大鼠中,A5去甲肾上腺素能神经元的损毁并未改变对低氧(7% O)和高碳酸血症(7% CO)的反射性心肺调节。在原位标本中,与对照相比,A5损毁大鼠由外周化学感受器刺激(ΔtSN:110±12% 对 58±8%,P<0.01)或高碳酸血症(ΔtSN:9.5±1.4% 对 3.9±1.7%,P<0.05)引发的交感兴奋减弱,但PN反射反应未减弱。我们的数据表明,A5去甲肾上腺素能神经元是未麻醉状态下参与处理对低氧和高碳酸血症交感反应的神经回路的一部分。