Tsai Hsiu-Wen, Davenport Paul W
Department of Physiological Sciences, University of Florida, Gainesville, Florida.
J Appl Physiol (1985). 2014 Apr 15;116(8):1006-16. doi: 10.1152/japplphysiol.01256.2013. Epub 2014 Feb 20.
Respiratory load compensation is a sensory-motor reflex generated in the brain stem respiratory neural network. The nucleus of the solitary tract (NTS) is thought to be the primary structure to process the respiratory load-related afferent activity and contribute to the modification of the breathing pattern by sending efferent projections to other structures in the brain stem respiratory neural network. The sensory pathway and motor responses of respiratory load compensation have been studied extensively; however, the mechanism of neurogenesis of load compensation is still unknown. A variety of studies has shown that inhibitory interconnections among the brain stem respiratory groups play critical roles for the genesis of respiratory rhythm and pattern. The purpose of this study was to examine whether inhibitory glycinergic neurons in the NTS were activated by external and transient tracheal occlusions (ETTO) in anesthetized animals. The results showed that ETTO produced load compensation responses with increased inspiratory, expiratory, and total breath time, as well as elevated activation of inhibitory glycinergic neurons in the caudal NTS (cNTS) and intermediate NTS (iNTS). Vagotomized animals receiving transient respiratory loads did not exhibit these load compensation responses. In addition, vagotomy significantly reduced the activation of inhibitory glycinergic neurons in the cNTS and iNTS. The results suggest that these activated inhibitory glycinergic neurons in the NTS might be essential for the neurogenesis of load compensation responses in anesthetized animals.
呼吸负荷补偿是一种在脑干呼吸神经网络中产生的感觉运动反射。孤束核（NTS）被认为是处理与呼吸负荷相关的传入活动的主要结构，并通过向脑干呼吸神经网络中的其他结构发送传出投射来促进呼吸模式的改变。呼吸负荷补偿的感觉通路和运动反应已经得到了广泛研究；然而，负荷补偿的神经发生机制仍然未知。各种研究表明，脑干呼吸组之间的抑制性相互连接对呼吸节律和模式的产生起着关键作用。本研究的目的是检查在麻醉动物中，NTS中的抑制性甘氨酸能神经元是否会被外部短暂气管阻塞（ETTO）激活。结果表明，ETTO产生了负荷补偿反应，吸气、呼气和总呼吸时间增加，同时尾侧NTS（cNTS）和中间NTS（iNTS）中抑制性甘氨酸能神经元的激活增强。接受短暂呼吸负荷的迷走神经切断动物未表现出这些负荷补偿反应。此外，迷走神经切断术显著降低了cNTS和iNTS中抑制性甘氨酸能神经元的激活。结果表明，NTS中这些被激活的抑制性甘氨酸能神经元可能对麻醉动物负荷补偿反应的神经发生至关重要。
