PARABRACHIAL NUCLEI--ROLE IN RESPIRATORY SYSTEM DEFENSE

对吸入有毒气雾剂的一种反应是突然终止 灵感。这种反射是由三叉神经支引起的。 支配鼻黏膜的神经。如果刺激性物质持续存在 上呼吸道或进入下呼吸道，则变化较为复杂 发生在呼吸模式中。形成这些的中央机制 综合反应综合反应，尤指三叉神经引起的反应 神经，却鲜为人知。我们假设桥脑 呼吸群(PRG)，位于嘴、背、背的双侧结构。 侧脑桥是大脑中脑的主要核团。 感官刺激进入中央模式生成器进行呼吸。 具体地说，我们认为PRG塑造了呼吸模式 对刺激鼻粘膜、喉和 胸腔内呼吸道受体。此外，我们假设PRG 与呼吸相关性较差的神经元更多 对感官刺激敏感，对变化更敏感 在意识状态下比那些高度活跃的神经元 受呼吸调节的。 我们提出了一套麻醉后的神经生理学实验 和未麻醉的猫，以确定呼吸道传入和PRG 活动通过吸气后神经元和 如果更复杂的呼吸模式重塑依赖于 PRG。我们将记录吸气、呼气和吸气后 运动单位活动并比较它们对刺激的反应 注射前后的三叉神经和喉上神经 在PRG中钴的含量。我们将刺激PRG的次区域 化学和电学并记录短潜伏期反应 延髓吸气后神经元和呼吸肌活动 以及呼吸计时(TI、TE、TTOT)。我们将使用量化 确定记录的PRG神经之间关系的方法 活动和呼吸。这种相关性反映了一种平衡 呼吸性和非呼吸性突触对神经元的驱动。 弱关联和调制不良的小区反映了优势 非呼吸系统的输入。 其目的是：1)比较肌肉和时序反应 突触阻断前后的呼吸道传入刺激 在PRG中的传播，2)决定呼吸道的模式 PRG微刺激引起的肌肉活动，3)分析 PRG神经元的活动模式，并将其行为与 它们对传入刺激和状态变化的反应 意识；4)分析延髓后反应。 吸气神经元，由喉上段兴奋的神经元 神经刺激，对三叉神经和PRG进行刺激。结果 将提供对神经生理学机制的洞察 PRG和呼吸道传入信息对延髓的影响 刺激、弱调制和强调制的PRG神经元和延髓 吸气后神经元。这种交互可能与 了解呼吸模式的变化与激活 炎症和炎症时的上、下呼吸道传入神经 令人恼火。

One response to inhaled noxious aerosols is an abrupt termination of inspiration. This reflex is elicited by the branch of trigeminal nerve that innervates the nasal mucosa. If irritants persist in the upper airway or enter the lower airway, then more complex changes occur in the breathing pattern. Central mechanisms forming these integrated responses, especially those elicited by the trigeminal nerve, are poorly understood. We hypothesize that the pontine respiratory group (PRG), a bilateral structure in the rostral, dorso- lateral pons, is a major nucleus necessary for the incorporation of sensory stimuli into the central pattern generator for respiration. Specifically, we believe that the PRG shapes the breathing pattern in response to stimulation of the nasal mucosal, laryngeal, and intrathoracic airway receptors. Furthermore, we hypothesize that PRG neurons that are poorly correlated with respiration are more responsive to sensory stimulation and are more sensitive to changes in state of consciousness than those neurons whose activity is highly modulated by respiration. We propose a set of neurophysiologic experiments in both anesthetized and unanesthetized cats to determine if airway afferent and PRG activities terminate inspiration through post-inspiratory neurons and if more complex reshaping of the breathing pattern is dependent on the PRG. We will record inspiratory, expiratory and post-inspiratory motor unit activity and compare their responses to stimulation of trigeminal and superior laryngeal nerves before and after injection of cobalt in the PRG. We will stimulate subregions of the PRG chemically and electrically and record short-latency responses of medullary post-inspiratory neuronal and respiratory muscle activity and of respiratory timing (TI,TE,TTOT). We will use quantitative methods for determining the relationship between recorded PRG neural activity and respiration. This correlation reflects a balance between respiratory and non-respiratory synaptic drive to a neuron. A weakly correlated and poorly modulated cell reflects a predominance of non-respiratory inputs. The aims are to: 1) compare the muscle and timing responses to airway-afferent stimulation before and after blocking synaptic transmission in the PRG, 2) determine the pattern of respiratory muscle activity elicited by microstimulation of the PRG, 3) analyze the activity patterns of PRG neurons and correlate their behavior to their responses to afferent stimulation and to changes in state of consciousness and 4) analyze the response of medullary post- inspiratory neurons, neurons that are excited by superior laryngeal nerve stimulation, to trigeminal nerve and PRG stimulation. Results will provide insight into the neurophysiologic mechanisms for influence of PRG and airway afferent information on medullary stimulation, weakly and strongly modulated PRG neurons, and medullary post-inspiratory neurons. Such interaction may be relevant to understanding changes in the breathing pattern with activation of upper and lower airway afferent nerves during inflammation and irritation.