MECHANISMS AND SITES OF VENTILATORY NEUROGENESIS

描述（改编自申请人的摘要）：自动 正常呼吸和喘息的解释模式可以从白天观察到， 出生。 在正常呼吸和喘息时，神经元和 神经活动是完全不同的。 在成年大鼠和猫中， 已经确定了一个髓区， 神经发生的喘息，但不是正常呼吸。 这个“喘息中心” 部分与区域重叠，称为“前Botzinger”复合体， “前I”区域，据报道包含神经元，其放电 是新生儿体外制备中节律产生的基础 大鼠 “喘息中心”、“前Botzinger”综合体和“前I”地区 可以表示连续的功能单元。 这种假设是 支持的身份的节奏活动的体外 通过在体内新生大鼠的喘息制备。 此外，在这些 新生动物，在各种延髓神经元的破坏 区域消除喘息，但不改变正常呼吸。 的作用 正常呼吸和喘息神经发生中的延髓神经元活动 将被评估。 将对这些机制进行评价， 延髓神经元的活动受到抑制， 呼吸正常 具体来说，脑桥神经元活动的放电是 被认为是这种压制的根源。 在正常呼吸中， 药理学“去抑制”和/或髓神经元的兴奋 活动应导致喘息。 拟议的研究将确定 正常呼吸节律的优势机制 是成立的。 研究结果将为理解 呼吸暂停时通气神经发生机制失败 新生儿和成人。

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.