NEUROGENESIS OF AUTOMATIC VENTILATORY ACTIVITY

我们提出了一系列相互关联的研究。在我的实验室中，假说将根据整体的通风活动进行评估。在为期四个月的三次访问期间，佩顿博士的实验室将使用细胞内分析对非常精确的假设进行测试。在第一次访问中，我们将描述呼吸调节放电的延髓神经元在呼吸暂停和喘息期间膜电位的变化。在真呼吸暂停中，整个呼吸周期的这些变化是由一系列复杂的兴奋和抑制电位定义的。我们将评估这样一种假设，即在喘息时，这些神经元的放电将主要或完全由兴奋性突触传递定义。在第二次访问期间，将检验一个相关的假设。阻断抑制性突触传递后，喘息周期中膜电位的变化不会改变。在第三次访问中，我们将确定一组延髓吸气神经元是否会出现典型的“起搏器神经元”的膜电位变化。这些起搏神经元的放电可能是喘息的神经发生的基础。在Eupnea中，这种起搏器放电被产生Eupnea节律的桥延髓神经元回路取代。

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 In eupnea, this pacemaker discharge is superseded by a pontomedullary neuronal circuit which generates the eupneic rhythm.