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% O2 every 3 min) or their normoxic (21% O2) 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 (IK) 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 IK 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.

中文翻译：

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慢性间歇性缺氧后内脏感觉神经元中催产素过度降低钾电流

来自下丘脑的催产素 (OT) 在几个心肺核中增加，并且在系统性地响应各种刺激和压力源，包括缺氧。在孤束核 (nTS) 内，心肺反射的第一个整合位点，OT 增强了突触传递、动作电位 (AP) 放电和心脏压力反射增益。缺氧压力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 从起源于结节神经节的压力传入神经元接收感觉输入。结节神经元表达 OT 受体 (OTR)，其激活可提高细胞内钙。然而，OT 对其他离子通道的影响，尤其是对 CIH 期间神经元活动重要的钾通道，鲜为人知。该研究试图确定 OT 正常和 CIH 后调节感觉传入-nTS 介导的反射的机制。来自雄性 Sprague-Dawley 大鼠的结节神经元在 10 天 CIH（每 3 分钟 6% O2）或它们的常氧 (21% O2) 对照后进行检查。在 Norm 和 CIH 神经节中鉴定出 OTR mRNA 和蛋白质，并且组间相似。为了检查 OTR 功能，在分离的神经元中记录了 AP 和钾电流 (IK)。与 Norm 相比，在 CIH OT 去极化神经元并减少电流诱导的 AP 放电后。在 CIH OT 之后，IK 也产生了更大的减少，而四乙基铵敏感的地方。这些数据表明，在 CIH OT 改变结节细胞中的离子电流后，可能会影响心肺反射和整体功能。