Speck D F, Feldman J L
J Neurosci. 1982 Jun;2(6):744-57. doi: 10.1523/JNEUROSCI.02-06-00744.1982.
The responses in respiratory outflow resulting from microstimulation and successive microlesions of the dorsal (DRG) and ventral (VRG) respiratory groups of neurons in the brainstem were studied in anesthetized, paralyzed, artificially ventilated cats. Microstimulation (2 to 120 Hz; 5 to 50 microA; 100 musec pulse duration) at almost every point within the DRG or VRG produced a bilateral short latency inhibition of phrenic nerve activity which had an onset latency of 4 to 9 msec and a duration of 4 to 24 msec. This global stereotyped phrenic inhibition was elicited by single pulses and often was accompanied by a postinhibitory excitation. In 48% (92/193) of the stimulation trials, trains of stimulus pulses during inspiration decreased the duration of inspiration. In 25% of the expiratory microstimulation trials, expiratory duration was increased and in 11%, expiration was shortened markedly by trains of pulses. Single shocks delivered to the right VRG or DRG produced a short latency excitation in the ipsilateral recurrent laryngeal nerve (RRL). This RRL excitation had an onset latency of 2 to 5 msec and a duration of 3 to 15 msec. Evidence suggests that the RRL excitation is due to a paucisynaptic activation of expiratory motoneurons in the caudal VRG. This activation is synchronous with the inhibition of inspiratory neurons in DRG and VRG. Despite the powerful short latency effects of microstimulation in VRG and DRG, extensive bilateral destruction of these neuronal populations had only modest effects on respiratory rhythm, while it decreased (or abolished) respiratory outflow in phrenic and recurrent laryngeal nerves. The combined results of the microstimulation and microlesion portions of this study suggest that a region (or regions) outside of the DRG and VRG might be important in the control of the respiratory pattern and that the DRG and VRG are important in determining the depth of inspiration; their role in generating respiratory rhythm needs to be critically re-examined.
在麻醉、麻痹并进行人工通气的猫身上,研究了脑干背侧(DRG)和腹侧(VRG)呼吸神经元群的微刺激及连续微损伤所引起的呼吸输出反应。在DRG或VRG内几乎每个点进行微刺激(2至120赫兹;5至50微安;100毫秒脉冲持续时间),都会产生双侧膈神经活动的短潜伏期抑制,起始潜伏期为4至9毫秒,持续时间为4至24毫秒。这种全身性的刻板膈神经抑制由单个脉冲引发,且常伴有抑制后兴奋。在48%(92/193)的刺激试验中,吸气期间的刺激脉冲串会缩短吸气持续时间。在25%的呼气微刺激试验中,呼气持续时间增加,而在11%的试验中,脉冲串会明显缩短呼气时间。对右侧VRG或DRG施加单次电击会在同侧喉返神经(RRL)产生短潜伏期兴奋。这种RRL兴奋的起始潜伏期为2至5毫秒,持续时间为3至15毫秒。有证据表明,RRL兴奋是由于尾侧VRG中呼气运动神经元的少突触激活所致。这种激活与DRG和VRG中吸气神经元的抑制同步。尽管微刺激对VRG和DRG有强大的短潜伏期效应,但对这些神经元群进行广泛的双侧破坏对呼吸节律的影响较小,不过会减少(或消除)膈神经和喉返神经的呼吸输出。本研究微刺激和微损伤部分的综合结果表明,DRG和VRG之外的一个或多个区域可能在呼吸模式控制中起重要作用,而DRG和VRG在决定吸气深度方面很重要;它们在产生呼吸节律中的作用需要重新进行严格审视。