HYPOTHALAMIC REGULATION OF RESPIRATION DURING SLEEP

许多证据支持下丘脑视前区(POA)的假设 温度敏感神经元在细胞周期调控中起着关键作用 NREM睡眠，作为整体代谢调节的一个组成部分。激活 POA温敏神经元的存在是启动的必要条件和充分条件 NREM睡眠。POA的催眠输出被假设为 抑制γ-氨基丁酸(GABA)能神经通路的下行 下丘脑后部(PH)和下丘脑后部的觉醒促进系统 脑干。在PH中，GABA调节的系统促进呼吸运动 和自主反应。我们假设PH的呼吸机制是 与PH唤醒的产生机制相结合，而唤醒诱导 起源于肺泡巨噬细胞的呼吸促进是 清醒--开车--呼吸。我们提出了一个模型，在这个模型中， 在睡眠期间被主动抑制，这种抑制起源于 POA，并由GABA能抑制投射从POA到 PH值。 拟议的研究将检验这一模型的核心假设。 POA温敏神经元的激活将1)抑制隔膜 和上呼吸道扩张器在睡眠中的活动以及2)抑制放电 慢性动物的PH神经元，通过GABA能过程。3)POA变暖 会降低延髓网状神经元的呼吸偶联。POA 降温将产生相反的效果。 阻塞性睡眠呼吸暂停以入睡诱导的呼吸道为特征 扩张器和呼吸泵肌肉失活。这些事件被认为是 是失去清醒驾驶到呼吸的后果。在……里面 此外，许多患者表现出唤醒反应减少和减少 对呼吸道阻力的补偿，因此，我们假设唤醒 调控失调是这种疾病的一部分。我们假设过多的能量 起源于POA的保育运动，会导致嗜睡和 睡眠开始时呼吸马达失活。

Much evidence supports a hypothesis that hypothalamic preoptic area (POA) temperature-sensitive neurons play a critical role in the regulation of NREM sleep, as a component of overall metabolic regulation. The activation of POA warm sensitive neurons is necessary and sufficient for initiation of NREM sleep. The hypnogenic output from the POA is hypothesized to be a descending gamma-aminobutyric acid (GABA)ergic pathway which inhibits arousal-promoting systems in the posterior hypothalamus (PH) and brainstem. In PH, a GABA-regulated system facilitates respiratory motor and autonomic responses. We hypothesize that PH respiratory mechanisms are coupled to PH arousal generating mechanisms, and that arousal induced respiratory facilitation originating in the PH is a critical component of the wakefulness-drive to-breathing. We propose a model in which this drive is actively inhibited during sleep, that this inhibition originates in the POA, and is mediated by GABAergic inhibitory projections from the POA to the PH. The proposed studies will examine hypothesis central to this model. Activation of POA warm-sensitive neurons will 1) suppress diaphragmatic and upper airway dilator activity during sleep and 2) suppress discharge of PH neurons in chronic animals, via a GABAergic process. 3) POA warming will reduce respiratory coupling of medullary reticular neurons. POA cooling will have opposite effects. Obstructive sleep apnea are characterize by sleep onset-induced airway dilator and respiratory pump muscle deactivation. These events are thought to be consequences of the loss of the wakefulness-drive-to-breathing. In addition, many patients exhibit reduced arousal responses and reduced compensation for airway resistance, Thus, we hypothesize that arousal dysregulation is part of the disease. We hypothesize that excessive energy conservation drive, originating in the POA, induces sleepiness and respiratory motor deactivation at sleep onset.