Department of Biomedical Sciences, Dalton Cardiovascular Research Center, University of Missouri, 134 Research Park Dr., Columbia, MO 65211, USA.
Auton Neurosci. 2020 Dec;229:102735. doi: 10.1016/j.autneu.2020.102735. Epub 2020 Sep 28.
Oxytocin (OT) from the hypothalamus is increased in several cardiorespiratory nuclei and systemically in response to a variety of stimuli and stressors, including hypoxia. Within the nucleus tractus solitarii (nTS), the first integration site for cardiorespiratory reflexes, OT enhances synaptic transmission, action potential (AP) discharge, and cardiac baroreflex gain. The hypoxic stressor obstructive sleep apnea, and its CIH animal model, elevates blood pressure and alters heart rate variability. The nTS receives sensory input from baroafferent neurons that originate in the nodose ganglia. Nodose neurons express the OT receptor (OTR) whose activation elevates intracellular calcium. However, the influence of OT on other ion channels, especially potassium channels important for neuronal activity during CIH, is less known. This study sought to determine the mechanism (s) by which OT modulates sensory afferent-nTS mediated reflexes normally and after CIH. Nodose ganglia neurons from male Sprague-Dawley rats were examined after 10d CIH (6% O every 3 min) or their normoxic (21% O) control. OTR mRNA and protein were identified in Norm and CIH ganglia and was similar between groups. To examine OTR function, APs and potassium currents (I) were recorded in dissociated neurons. Compared to Norm, after CIH OT depolarized neurons and reduced current-induced AP discharge. After CIH OT also produced a greater reduction in I that where tetraethylammonium-sensitive. These data demonstrate after CIH OT alters ionic currents in nodose ganglia cells to likely influence cardiorespiratory reflexes and overall function.
下丘脑的催产素（OT）在多种刺激和应激源（包括缺氧）作用下，会在几个心肺呼吸核团中增加，并在全身增加。在孤束核（nTS）中，心肺反射的第一个整合部位，OT 增强了突触传递、动作电位（AP）放电和心脏压力反射增益。缺氧应激源阻塞性睡眠呼吸暂停及其 CIH 动物模型会升高血压并改变心率变异性。nTS 接收来自结状神经节的压力感受器神经元的感觉输入。结状神经元表达 OT 受体（OTR），其激活会增加细胞内钙。然而，OT 对其他离子通道的影响，特别是对 CIH 期间神经元活动很重要的钾通道，知之甚少。这项研究旨在确定 OT 调节感觉传入- nTS 介导的反射的机制（s），无论是在正常情况下还是在 CIH 之后。雄性 Sprague-Dawley 大鼠的结状神经节神经元在接受 10d CIH（每 3 分钟 6%O）或其正常氧（21%O）对照后进行了检查。在 Norm 和 CIH 神经节中鉴定了 OTR mRNA 和蛋白，两组之间相似。为了检查 OTR 功能，在分离的神经元中记录了 AP 和钾电流（I）。与 Norm 相比，CIH 后 OT 使神经元去极化并减少电流诱导的 AP 放电。CIH 后，OT 还产生了更大的减少，其中四乙铵敏感。这些数据表明，CIH 后 OT 改变了结状神经节细胞中的离子电流，可能会影响心肺反射和整体功能。
