NEURAL MECHANISMS OF APNEA

虽然新生儿的呼吸调节有许多相似之处 成虫在数量和质量上存在差异。这是有可能的 这些发育差异解释了明显的 新生儿对延长的自发性呼吸暂停的易感性。这个 目前的研究是基于这样一种假设：中枢神经机制 在呼吸调节方面比传统上更重要 被认可了。长期目标是发展对中央的理解 破坏呼吸动力稳定的神经机制。具体的 这项研究的目标是开发技术并确保可行性 使用脑干呼吸神经元细胞内记录的项目 发育中的动物。 不同细胞内呼吸相关活动的细胞内记录 将进行人口调查，以确定导致 刺激后持续的呼吸效应。已经开发了一个模型 证明起源于喉上神经的反射 诱导吸气后神经元的长时间活动。这些神经元是 在从吸气到呼气的阶段转换过程中表现出显著的活跃。 因此，这些神经元的长时间激活可能是 呼吸暂停。为了进一步描述这一机制，本文提出了两项研究。 第一项研究是调查激活的机制 吸气后的细胞会导致吸气神经元的静止。第二， 上呼吸道刺激导致延长时间的方法 吸气后的激活将被确定。第二项研究是 专为区分1)直接和间接而设计 吸气后细胞的突触激活，以及2)是否延长 刺激后神经元活动是由于持续的突触刺激或 膜电导发生变化。这两项研究将在#年完成 成年猫。 本项目的第三部分是确定 应用这一技术研究中部地区的发展问题 呼吸活动的神经元整合。目前还没有 对于这种类型的研究，存在一个既定的模型。上述两项研究 在海德堡大学生理学研究所表演 将为类似研究的应用提供技术框架 新生儿将在该项目的第二年执行。 抑制性反射的中枢整合可能具有重要意义 对于患有呼吸暂停的早产儿，较大的婴儿有猝发的风险 婴儿死亡综合征，以及婴儿和成人阻塞性睡眠 呼吸暂停。

Though respiratory regulation in newborns has many similarities with adults, quantitative and qualitative differences exist. It is possible that these developmental differences account for the pronounced susceptibility of newborn infants to have prolonged spontaneous apnea. The present studies are based on the hypothesis that central neural mechanisms are more important in respiratory regulation than traditionally recognized. The long-range goal is to develop an understanding of central neural mechanisms that destabilize respiratory drive. The specific objective of this study is to develop techniques and assure feasibility for projects using intracellular recording of brainstem respiratory neurones in developing animals. Intracellular recording of respiratory-related activity in different cell populations will be undertaken to determine cellular mechanisms which lead to prolonged post-stimulus respiratory effects. A model has been developed demonstrating that reflexes originating in the superior laryngeal nerve induce prolonged activity in post-inspiratory neurones. These neurones are prominently active during phase switching from inspiration to expiration. Therefore, prolonged activation of these neurones is a likely mechanism of apnea. Two studies are proposed to further characterize this mechanism. The first study is to investigate the mechanisms by which activation of post-inspiratory cells cause inspiratory neurone quiesence. Second, the means by which upper airway stimulation results in prolonged post-inspiratory activation will be determined. The second study is designed specifically to distinguish between 1) direct and indirect synaptic activation of post-inspiratory cells, and 2) whether prolonged post-stimulus neuronal activity is due to continued synaptic stimulation or membrane conductance changes. These two studies are to be accomplished in adult cats. The third portion of this project is to determine the feasibility of applying this technology to study of developmental aspects of central neuronal integration of respiratory activity. There does not currently exist an established model for this type of study. The above two studies performed at the Physiologisches Institut of the Universitat Heidelberg will provide the technical framework for application of similar studies in newborns to be performed during this project's second year. Central integration of inhibitory reflexes may have important implications for premature newborns with apnea, older infants at risk for the Sudden Infant Death Syndrome, as well as infants and adults with obstructive sleep apnea.