NEUROGENESIS OF AUTOMATIC VENTILATORY ACTIVITY

我们提出了一系列相互关联的研究。在我的实验室里，假设将根据总体解释活动来评估。在为期四个月的三次访视期间，将在Paton博士的实验室使用细胞内分析进行非常精确的假设检验。在第一次访问中，我们将描述具有呼吸调节放电的延髓神经元在正常呼吸和喘息期间膜电位的变化。在正常呼吸中，整个呼吸周期的这些变化由一系列复杂的兴奋性和抑制性电位定义。我们将评估的假设，在喘息，这些神经元的放电将主要或完全由兴奋性突触传递定义。将在第二次访视期间检验相关假设。阻断抑制性突触传递后，喘息周期中膜电位的变化将保持不变。在第三次访视期间，我们将确定一组延髓吸气神经元是否会发生典型的“起搏神经元”膜电位变化。“这些起搏神经元的放电可能是喘息的神经发生的基础。在正常呼吸中，这种起搏放电被产生正常呼吸节律的脑桥延髓神经元回路所取代。

We propose a series of interrelated studies. In my laboratory, hypotheses will be evaluated in terms of overall ventilatory activity. During three visits each of four months duration, testing of very precise hypotheses will then be performed in Dr. Paton's laboratory using intracellular analyses. In the first visit, we will characterize changes in the membrane potentials during eupnea and gasping of medullary neurons having respiratory-modulated discharges. In eupnea, these changes throughout the respiratory cycle are defined by a complex series of excitatory and inhibitory potentials. We will evaluate the hypothesis that, in gasping, the discharge of these neurons will be defined largely or exclusively by excitatory synaptic transmission. A related hypothesis will be tested during the second visit. The changes of membrane potentials during the gasping cycle will be unaltered following a blockade of inhibitory synaptic transmission. During the third visit, we will define if a group of medullary inspiratory neurons will have changes in membrane potential typical of "pacemaker neurons." The discharge of these pacemaker neurons may underlie the neurogenesis of the gasp. In eupnea, this pacemaker discharge is superseded by a pontomedullary neuronal circuit which generates the eupneic rhythm.