Feldman J L, McCrimmon D R, Speck D F
J Physiol. 1984 Feb;347:241-54. doi: 10.1113/jphysiol.1984.sp015064.
The effects on phrenic nerve discharge elicited by intraspinal stimulation which produced synchronous activation of bulbo-spinal inspiratory neurones were investigated in chloralose-urethane anaesthetized, paralysed, vagotomized and artificially ventilated cats. Descending respiratory axons were activated in the ventrolateral spinal cord at the second cervical level using either monopolar or bipolar stimulation (25-200 microA, 100 microseconds, 1-300 Hz). Activation of bulbo-spinal axons was confirmed by recording both orthodromic phrenic nerve excitation and antidromic spike invasion of single, inspiratory modulated units in either the dorsal respiratory group (d.r.g.) or ventral respiratory group (v.r.g.). Antidromic activation of inspiratory bulbo-spinal neurones was confirmed by the criteria of high frequency following and collision tests. Spinal cord stimulation at intensities of 100 microA antidromically activated approximately half of the inspiratory bulbo-spinal neurones in the d.r.g. and v.r.g. Stimulation pulses delivered to the spinal cord elicited an orthodromic excitation of the ipsilateral phrenic nerve lasting 2-12 ms during inspiration. The onset latency of excitation was 2-4 ms, decreasing as inspiration progressed. Following the initial excitation there was a 4-30 ms period of reduced phrenic nerve discharge. Continuous trains of stimuli (less than 100 microA, 100 microseconds, 1-300 Hz) or phrenic gated trains delivered during every fourth inspiratory or expiratory cycle had little or no effect on the duration of inspiration or expiration. Brief trains (400 ms, 50 Hz, 100 microA) of bilateral spinal cord stimulation delivered at various delays from the onset of inspiration had only a transient effect on the pattern of phrenic nerve discharge, with no noticeable effect 60 ms after termination of stimulation. Based on the assumption that synchronous activation of a portion of the central pattern generator for respiration would phase shift or reset the rhythm, we conclude that the bulbo-spinal inspiratory neurones are not responsible for generation of respiratory timing signals and play, at most, a limited role in the generation of the augmenting central inspiratory activity.
在氯醛糖 - 乌拉坦麻醉、麻痹、切断迷走神经并人工通气的猫身上，研究了脊髓内刺激引发的膈神经放电效应，该刺激可使延髓 - 脊髓吸气神经元同步激活。在第二颈椎水平的脊髓腹外侧，使用单极或双极刺激（25 - 200微安，100微秒，1 - 300赫兹）激活下行呼吸轴突。通过记录背侧呼吸组（d.r.g.）或腹侧呼吸组（v.r.g.）中单个吸气调制单元的正向膈神经兴奋和逆向锋电位入侵，证实了延髓 - 脊髓轴突的激活。通过高频跟随和碰撞试验标准，证实了吸气性延髓 - 脊髓神经元的逆向激活。强度为100微安的脊髓刺激逆向激活了d.r.g.和v.r.g.中约一半的吸气性延髓 - 脊髓神经元。在吸气期间，传递到脊髓的刺激脉冲引发同侧膈神经持续2 - 12毫秒的正向兴奋。兴奋的起始潜伏期为2 - 4毫秒，随着吸气进行而缩短。在初始兴奋之后，有一个4 - 30毫秒的膈神经放电减少期。连续的刺激序列（小于100微安，100微秒，1 - 300赫兹）或在每第四个吸气或呼气周期中给予的膈门控刺激序列对吸气或呼气的持续时间几乎没有影响。在吸气开始后的不同延迟时间给予短暂的双侧脊髓刺激序列（400毫秒，50赫兹，100微安），对膈神经放电模式只有短暂影响，刺激终止60毫秒后无明显影响。基于呼吸中枢模式发生器的一部分同步激活会使节律发生相移或重置的假设，我们得出结论，延髓 - 脊髓吸气神经元不负责呼吸定时信号的产生，并且在增强中枢吸气活动的产生中最多只起有限作用。
