CNS PROCESSING OF BRONCHOPULMONARY FIBER AFFERENT INPUT

肺和呼吸道中的支气管肺泡炎C纤维受体 将感觉信息传递到中枢神经系统以调节呼吸模式。 的 受体被肺自体激素如缓激肽刺激， 外源性化学物质，如苯二胍（一种血清素 结构类似物）和辣椒素;环境毒物如臭氧 和香烟烟雾以及严重的肺水肿 刺激时 支气管肺纤维素C受体产生快速浅呼吸 (that可能先有呼吸暂停）、心动过缓、低血压和 增加气道阻力。 这项研究的长期目标是 表征支气管肺纤维化C的激活 纤维感受器反射性地产生快速的浅呼吸模式。 我们 已经确定了在离散的反射通路中的近端突触， 孤束核（NTS）的区域（6）。 我们还收集了 关于远端突触的初步数据，这表明传入 来自支气管肺纤维素C受体的输入最终调节 腹侧呼吸组（VRG）神经元的活动。 我们假设 为了产生快速浅呼吸，支气管肺泡C纤维传入 输入会聚到连合NTS中的离散区域中的神经元上， 然后分叉，以兴奋在早期放电的嘴侧VRG中的神经元， 以递减模式到期（早期E或EDEC细胞）。 这些 早期（EDEC）细胞，反过来又抑制球脊髓吸气（I）细胞（以 降低膈神经活动的幅度和爆发持续时间），以及 抑制尾侧VRG中在呼气晚期放电的E细胞（晚期E 细胞）和支配脊髓中的呼气运动神经元（以 减少呼气时间）。 研究将在麻醉大鼠中进行，我们记录 CNS中的细胞外单个单位活动，膈神经活动， 潮气量和系统动脉压。 支气管平滑肌C纤维 受体将通过将PDG注射到右心房中而被刺激。 的 目的是：1）确定，使用细胞外记录，如果神经元在 NTS区域（先前表征; 6）接收来自 支气管肺泡灌洗液C纤维受体; 2）确定 支气管肺泡C纤维受体刺激对肺动脉平滑肌细胞放电模式的影响 VRG吻侧的早期E细胞（EDEC）和Botzinger复合体，I细胞 整个VRG，和尾VRG中的晚期E细胞;并确定， 使用逆向激活，这些细胞的投射，即向 膈运动核、胸脊髓、迷走神经或上级 喉神经（SLN）; 3）确定，使用互相关分析，

Bronchopulmonary C fiber receptors in the lungs and airways transmit sensory information to the CNS to modulate respiratory pattern. The receptors are stimulated by lung autacoids such as bradykinin and prostaglandins; by exogenous chemicals such as phenyldiguanide (a serotonin structural analog) and capsaicin; by environmental toxicants such as ozone and cigarette smoke, and during severe pulmonary edema. When stimulated the bronchopulmonary C fiber receptors produce rapid shallow breathing (that may be preceded by an apnea), bradycardia, hypotension, and an increase in airway resistance. The long-term goal of this research is to characterize the central circuitry whereby activation of bronchopulmonary C fiber receptors reflexly produces a rapid shallow pattern of breathing. We have identified proximal synapse(s) in the reflex pathway in a discrete region in the nucleus tractus solitarius (NTS) (6). We have also collected preliminary data regarding distal synapses, which suggest that afferent input from the bronchopulmonary C fiber receptors ultimately modulates the activity of neurons in the ventral respiratory group (VRG). We hypothesize that to produce rapid shallow breathing, bronchopulmonary C fiber afferent input converges onto neurons in a discrete region in commissural NTS and then diverges to excite neurons in the rostral VRG that discharge in early expiration with a decrementing pattern (early E or EDEC cells). These early (EDEC) cells, in turn inhibit bulbospinal inspiratory (I) cells (to decrease the amplitude and burst duration of phrenic nerve activity), and inhibit E cells in the caudal VRG that discharge in late expiration (late E cells) and that innervate expiratory motoneurons in the spinal cord (to decrease expiratory time). Studies will be performed in urethane-anesthetized rats in which we record extracellular single unit activity in the CNS, phrenic nerve activity, tidal volume, and systematic arterial pressure. Bronchopulmonary C fiber receptors will be stimulated by injecting PDG into the right atrium. The aims are: 1) to determine, using extracellular recording, if neurons in the NTS region (previously characterized; 6) receive excitatory input from bronchopulmonary C fiber receptors; 2) to determine the effects of bronchopulmonary C fiber receptor stimulation on the discharge patterns of early E cells (EDEC) in the rostral VRG and Botzinger complex, I cells throughout the VRG, and late E cells in the caudal VRG; and to determine, using antidromic activation, the projections of those cells, i.e. to the phrenic motor nucleus, thoracic spinal cord, vagus nerve, or the superior laryngeal nerve (SLN); 3) to determine, using cross-correlation analysis,