Solomon I C, Edelman N H, Neubauer J A
Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, New Jersey 08903-0019, USA.
J Neurophysiol. 1999 Mar;81(3):1150-61. doi: 10.1152/jn.1999.81.3.1150.
The pre-Bötzinger complex (pre-BötC) has been proposed to be essential for respiratory rhythm generation from work in vitro. Much less, however, is known about its role in the generation and modulation of respiratory rhythm in vivo. Therefore we examined whether chemical stimulation of the in vivo pre-BötC manifests respiratory modulation consistent with a respiratory rhythm generator. In chloralose- or chloralose/urethan-anesthetized, vagotomized cats, we recorded phrenic nerve discharge and arterial blood pressure in response to chemical stimulation of neurons located in the pre-BötC with DL-homocysteic acid (DLH; 10 mM; 21 nl). In 115 of the 122 sites examined in the pre-BötC, unilateral microinjection of DLH produced an increase in phrenic nerve discharge that was characterized by one of the following changes in cycle timing and pattern: 1) a rapid series of high-amplitude, rapid rate of rise, short-duration bursts, 2) tonic excitation (with or without respiratory oscillations), 3) an integration of the first two types of responses (i.e., tonic excitation with high-amplitude, short-duration bursts superimposed), or 4) augmented bursts in the phrenic neurogram (i.e., eupneic breath ending with a high-amplitude, short-duration burst). In 107 of these sites, the phrenic neurogram response was accompanied by an increase or decrease (>/=10 mmHg) in arterial blood pressure. Thus increases in respiratory burst frequency and production of tonic discharge of inspiratory output, both of which have been seen in vitro, as well as modulation of burst pattern can be produced by local perturbations of excitatory amino acid neurotransmission in the pre-BötC in vivo. These findings are consistent with the proposed role of this region as the locus for respiratory rhythm generation.
前包钦格复合体（pre - BötC）被认为对体外实验中呼吸节律的产生至关重要。然而，关于其在体内呼吸节律的产生和调节中的作用，人们所知甚少。因此，我们研究了体内前包钦格复合体的化学刺激是否表现出与呼吸节律发生器一致的呼吸调节作用。在氯醛糖或氯醛糖/氨基甲酸乙酯麻醉、切断迷走神经的猫中，我们记录了膈神经放电和动脉血压，以响应使用DL - 高半胱氨酸（DLH；10 mM；21 nl）对位于前包钦格复合体中的神经元进行的化学刺激。在前包钦格复合体检查的122个位点中的115个位点，单侧微量注射DLH导致膈神经放电增加，其特征在于周期时间和模式有以下变化之一：1）一系列快速的高振幅、快速上升速率、短持续时间的爆发；2）强直兴奋（伴有或不伴有呼吸振荡）；3）前两种反应类型的整合（即伴有叠加的高振幅、短持续时间爆发的强直兴奋）；或4）膈神经电图中的增强爆发（即平静呼吸以高振幅、短持续时间爆发结束）。在这些位点中的107个位点，膈神经电图反应伴有动脉血压升高或降低（≥10 mmHg）。因此，呼吸爆发频率增加和吸气输出的强直放电产生，这两者在体外实验中均已观察到，以及爆发模式的调节，可以通过体内前包钦格复合体中兴奋性氨基酸神经传递的局部扰动来产生。这些发现与该区域作为呼吸节律产生位点的推测作用一致。
