This study addressed the hypothesis that there is a parallel processing of input from carotid chemoreceptors to brainstem neurones involved in inspiratory phase timing and control of inspiratory motor output amplitude. Data were from fifteen anaesthetized, bilaterally vagotomized, paralysed, artificially ventilated cats. Carotid chemoreceptors were stimulated by close arterial injection of 200 microliters of CO2-saturated saline solution. 2. Planar arrays of tungsten microelectrodes were used to monitor simultaneously up to twenty-two neurones in the nucleus tractus solitarii (NTS) and ventral respiratory group (VRG). Spike trains were analysed with two statistical tests of respiratory modulation, cycle-triggered histograms, peristimulus-time histograms, cumulative sum histograms and cross-correlograms. 3. In NTS, 16 of 26 neurones with respiratory and 12 of 27 without respiratory modulation changed firing rate during carotid chemoreceptor stimulation. In the VRG 72 of 112 respiratory and 14 of 48 non-respiratory neurones changed firing rate during stimulation. 4. The spike trains of 85 of 1276 pairs (6.7%) of cells exhibited short time scale correlations indicative of paucisynaptic interactions. Ten pairs of neurones were each composed of a rostral VRG phasic inspiratory neurone that responded to carotid chemoreceptor stimulation with a decline in firing rate and a caudal VRG phasic inspiratory neurone that increased its firing rate. Cross-correlograms from two of the pairs had features consistent with excitation of the caudal neurones by the rostral cells. A decrease in the duration of activity of the rostral VRG neurones was paralleled by the decrease in inspiratory time of phrenic nerve activity. Caudal VRG inspiratory neurones increased their activity as phrenic amplitude increased. Spike-triggered averages of all four neurones indicated post-spike facilitation of phrenic motoneurones. 5. The results support the hypothesis that unilateral stimulation of carotid chemoreceptors results in parallel actions. (a) Inhibition of rostral VRG I-Driver neurones decreases inspiratory duration. (b) Concurrent excitation of premotor VRG and dorsal respiratory group inspiratory neurones increases inspiratory drive to phrenic motoneurones. Other data suggest that responsive ipsilateral neurones act to regulate contralateral neurones.
摘要
本研究探讨了以下假说:来自颈动脉化学感受器的输入信息会并行处理至参与吸气相定时和吸气运动输出幅度控制的脑干神经元。数据来自15只麻醉、双侧迷走神经切断、麻痹、人工通气的猫。通过向动脉内近距离注射200微升二氧化碳饱和盐溶液来刺激颈动脉化学感受器。2. 使用钨微电极平面阵列同时监测孤束核(NTS)和腹侧呼吸组(VRG)中多达22个神经元。通过两种呼吸调制统计测试、周期触发直方图、刺激时间直方图、累积和直方图以及互相关图来分析脉冲序列。3. 在NTS中,26个有呼吸调制的神经元中有16个以及27个无呼吸调制的神经元中有12个在颈动脉化学感受器刺激期间放电率发生变化。在VRG中,112个有呼吸调制的神经元中有72个以及48个无呼吸调制的神经元中有14个在刺激期间放电率发生变化。4. 1276对细胞中的85对(6.7%)的脉冲序列表现出短时间尺度的相关性,表明存在少突触相互作用。有十对神经元,每对均由一个延髓VRG相位性吸气神经元和一个尾侧VRG相位性吸气神经元组成,前者对颈动脉化学感受器刺激的反应是放电率下降,后者的放电率则增加。其中两对神经元的互相关图具有与延髓细胞对尾侧神经元的兴奋作用相一致的特征。延髓VRG神经元活动持续时间的减少与膈神经活动吸气时间的减少并行出现。随着膈神经幅度增加,尾侧VRG吸气神经元的活动增加。所有四个神经元的脉冲触发平均值表明膈运动神经元在脉冲发放后出现易化。5. 结果支持以下假说:单侧刺激颈动脉化学感受器会产生并行作用。(a)抑制延髓VRG I -驱动神经元会缩短吸气持续时间。(b)同时兴奋运动前VRG和背侧呼吸组吸气神经元会增加对膈运动神经元的吸气驱动。其他数据表明,有反应的同侧神经元会对调节对侧神经元起作用。