MECHANISMS AND SITES OF VENTILATORY NEUROGENESIS

描述(摘自申请者的摘要)：“自动”呼吸 在没有有意识的努力下发生的运动，是在 脑干的桥脑和延髓部分。有几种模式 “自动”通风。Eupnea是“正常”的呼吸。在Eupnea，足够 氧气供应给身体，二氧化碳被排出，以满足新陈代谢 要求。如果真呼吸停止，就会出现缺氧。严重缺氧新兵 喘息，这是一种强大的防御机制 “自动复苏”一个根本的问题涉及到具体的 产生呼吸暂停和喘息的神经生理机制。严重者 低氧时，假设有一种潜在的起搏器放电的延髓 呼吸神经元被释放以产生喘息。在Eupnea，这个起搏器 活动并入负责脑桥延髓的神经元回路。 对于真核呼吸暂停的神经发生。神经生理学的定义 负责此次合并的流程将增强我们对 Eupnea本身的神经发生。建议的研究需要可逆的 呼吸暂停变为喘息。此外，为了评估这一机制的作用 各种可能的神经递质在呼吸性神经发生中的作用 药物将系统地给药，并通过以下方式给神经元 微离子导入。灌流的“幼鼠”特别适合 这些研究的成功实施。因为全身性的“呼吸”和 这种制剂的“循环系统”被体外循环“取代”。 电路，在低氧诱导过程中不存在心力衰竭的可能性 气喘吁吁。同样，可以使用药理药物，这将 几乎肯定会损害心血管功能和体内生存能力 准备工作。这些研究的结果将为 产生正常呼吸的机制。这样的信息可能 提供了对人类通风控制功能障碍的见解， 比如“睡眠呼吸暂停综合症”或“婴儿猝死综合症”。

DESCRIPTION (Adapted from the applicant's abstract):"Automatic" breathing movements, which occur without conscious effort, are generated within the pontile and medullary portions of the brainstem. There are several patterns of "automatic" ventilation. Eupnea is "normal" breathing. In eupnea, sufficient oxygen is supplied to the body and carbon dioxide removed to meet metabolic demands. If eupnea ceases, hypoxia will develop. Severe hypoxia recruits gasping, which serves as a powerful defensive mechanism for "autoresuscitation." A fundamental question concerns the specific neurophysiological mechanisms which generate eupnea and gasping. In severe hypoxia, it is hypothesized that a latent pacemaker discharge of medullary respiratory neurons is released to generate the gasp. In eupnea, this pacemaker activity is incorporated into the pontomedullary neuronal circuits responsible for the neurogenesis of eupnea. A definition of the neurophysiological processes responsible for this incorporation will enhance our understanding of the neurogenesis of eupnea, per se. The studies proposed require the reversible alteration of eupnea to gasping. Moreover, in order to evaluate the role of various putative neurotransmitters in ventilatory neurogenesis, pharmacological agents will be administered systemically, as well as onto neurons by microiontophoresis. The perfused "juvenile rat" is uniquely suited for the successful performance of these studies. Since the systemic "respiratory" and "circulatory" systems of this preparation are "replaced" by an extracorporeal circuit, there is no possibility of cardiac failure during hypoxia-induced gasping. Likewise, pharmacological agents can be administered which would almost certainly compromise cardiovascular function and viability of an in vivo preparation. Results of these studies will provide significant information into the mechanisms by which normal breathing is generated. Such information might provide insights into dysfunctions of the control of ventilation in humans, such as in "sleep apneas" or the "sudden infant death syndrome."