Bongianni F, Fontana G, Pantaleo T
Dipartimento di Scienze Fisiologiche, Università di Firenze, Italy.
Brain Res. 1988 Apr 5;445(2):254-61. doi: 10.1016/0006-8993(88)91187-0.
The effects of electrical and chemical stimulation of the expiratory neuronal population in the region of the retrofacial nucleus, the so called 'Bötzinger complex' (Böt. c.), on respiratory activity were investigated in vagotomized cats under pentobarbitone anaesthesia. Some of the experiments were performed on paralyzed or bilaterally thoracotomized, artificially ventilated animals. Sustained tetanic electrical stimulation (20 to 100-Hz, 0.5-ms current pulses at intensities of 5-60 microA) induced strong depressant effects on the inspiratory motor output which could lead to complete apnoea. The apnoeic response was accompanied by tonic activation of expiratory muscles; the appearance and the strength of tonic expiratory activity were dependent upon the frequency of stimulation. Brief tetani (40 to 100 ms trains of 0.5-ms rectangular pulses at 100-300 Hz) timed either during the inspiratory or the expiratory phase caused depression of inspiratory activity and prolongation of expiratory time, respectively. These effects increased gradually as the onset of stimulation was progressively delayed during each respiratory phase. The effects of sustained tetanic stimulation were mimicked by microinjections (25-100 nl) of 0.5 M L-glutamate or 0.16 M DL-homocysteic acid in the same region, thus indicating that they were the result of the stimulation of cell bodies and not of axons of passage. The present results support the hypothesis that Böt. c. neurons play an important role in the control of the breathing pattern by exerting inhibitory influences on inspiratory activity and, possibly, by contributing to the off-switch mechanisms. Furthermore, they suggest that these neurons are involved in the central control of expiratory activity.
在戊巴比妥麻醉下，对迷走神经切断的猫研究了在面神经后核区域（即所谓的“包钦格复合体”，Böt.c.）对呼气神经元群进行电刺激和化学刺激对呼吸活动的影响。部分实验是在瘫痪或双侧开胸、人工通气的动物身上进行的。持续的强直电刺激（20至100赫兹，0.5毫秒电流脉冲，强度为5至60微安）对吸气运动输出产生强烈的抑制作用，可导致完全呼吸暂停。呼吸暂停反应伴有呼气肌的强直性激活；强直性呼气活动的出现和强度取决于刺激频率。在吸气期或呼气期定时给予短暂的强直刺激（100至300赫兹的0.5毫秒矩形脉冲串，持续40至100毫秒）分别导致吸气活动抑制和呼气时间延长。随着刺激在每个呼吸阶段的开始逐渐延迟，这些效应逐渐增强。在同一区域微量注射（25至100纳升）0.5M的L-谷氨酸或0.16M的DL-高半胱氨酸可模拟持续强直刺激的效应, 这表明这些效应是刺激细胞体而非传导轴突的结果。目前的结果支持这样的假设，即Böt.c.神经元通过对吸气活动施加抑制性影响，以及可能通过参与关闭机制，在呼吸模式的控制中发挥重要作用。此外，这些结果表明这些神经元参与了呼气活动的中枢控制。
