MECHANISMS AND SITES OF VENTILATORY NEUROGENESIS

描述(改编自申请人的摘要)：自动 从白天开始就可以观察到呼吸暂停和喘息的模式。 出生地。在真呼吸暂停和喘息时，神经元和 神经活动从根本上说是不同的。在成年老鼠和猫身上， 已经确定了一个髓质区域，它对 喘息的神经发生，但不是真呼吸。这个“喘息中心” 与区域部分重叠，被称为“前波辛格”复合体 “Pre-I”区，据报道含有放电的神经元 新生儿体外准备中节律产生的基础 老鼠。“喘息中心”、“前波辛格”情结和“前I”区 可以代表一个连续的功能单元。这一假设是 由体外节律活动的同一性支持 活体新生大鼠喘气准备。而且，在这些方面， 新生动物，各种延髓内神经元的破坏 区域消除了喘息，但不会改变呼吸暂停。的角色 延髓神经元活动在真呼吸暂停和喘息神经发生中的作用 将会被评估。将对这些机制进行评估， 喘息背后的延髓神经元活动受到抑制 真核生物。具体地说，脑桥神经元活动的放电是 被认为是这种镇压的根源。在Eupnea， 延髓神经元的药理“去抑制”和/或兴奋 活动应该导致喘不过气来。建议的研究将定义 常温呼吸节律占优势的机制 已经确立了。这些结果将为理解 呼吸暂停中呼吸性神经发生机制的失败 新生儿和成年人。

DESCRIPTION (Adapted from the applicant's abstract): The automatic ventilatory patterns of eupnea and gasping can be observed from the day of birth. In eupnea and gasping, the discharge patterns of neuronal and neural activities are fundamentally different. In adult rats and cats, a medullary region has been identified which is critical for the neurogenesis of gasping, but not eupnea. This "gasping center" partially overlaps with regions, termed the "pre-Botzinger" complex and "Pre-I" region, which are reported to contain neurons whose discharge underlies rhythm generation in an in vitro preparation of the neonatal rat. The "gasping center", "pre-Botzinger" complex and "Pre- I" region may represent a continuous functional unit. This hypothesis is supported by the identity of the rhythmic activity of the in vitro preparation with gasping of in vivo neonatal rats. Moreover, in these neonatal animals, destruction of neurons in the various medullary regions eliminates gasping, but does not alter eupnea. The roles of medullary neuronal activities in the neurogenesis of eupnea and gasping will be assessed. The mechanisms will be evaluated by which these medullary neuronal activities underlying gasping are suppressed in eupnea. Specifically, the discharge of pontile neuronal activities is considered as the source of this suppression. In eupnea, pharmacological "disinhibition" and/or excitation of medullary neuronal activities should result in gasping. The studies proposed will define the mechanisms whereby the dominance of the eupneic ventilatory rhythm is established. Results will provide a basis for understanding the failure of mechanisms for ventilatory neurogenesis, in apneas of neonates and adults.