Behavior of VRG neurons during the atonia of REM sleep induced by pontine carbachol in decerebrate cats.
Behavior of VRG neurons during the atonia of REM sleep induced by pontine carbachol in decerebrate cats.
复制标题
VRG 神经元在去大脑猫中由脑桥卡巴胆碱诱导的快速眼动睡眠失张力过程中的行为。
DOI：
10.1016/0006-8993(92)91662-x
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发表时间：
1992
期刊：
影响因子：
2.9
通讯作者：
Davies,RO
中科院分区：
文献类型：
--
作者：
Kubin,L;Kimura,H;Tojima,H;Pack,AI;Davies,RO
将卡巴胆碱微量注射到急性去大脑猫的脑桥中，引起快速眼动睡眠样的张力和呼吸运动神经元活动的严重抑制(J.Appl。PhysIOL，69(1990)2280-2289)。为了探讨这种抑制是否由延髓神经元为呼吸泵肌(横隔肌和肋间)的运动神经元提供呼吸驱动所介导，我们研究了桥脑卡巴胆碱对去大脑、迷走神经切断、瘫痪和人工呼吸机猫腹侧呼吸组(VRG)神经元活动的影响。细胞外记录VRG神经元，并记录膈神经和肋间神经(外神经和内神经)的活动。吸气(I)和呼气(E)VRG神经元在它们的放电期都有递增的、斜坡状的活动爆发，而不是迷走神经运动神经元。卡巴胆碱抑制了大多数被研究神经元(42/57)的峰值放电频率。然而，尽管运动神经元水平持续抑制，但5个细胞没有变化，10个细胞活性增加。细胞总数(34I和23E)的放电峰值降低到88.5%±16.3(S.D.)对控制权的控制。同时记录到的膈活动减少到对照组的77.9%±11.5，吸气肋间活动减少到63.4%±21.6，呼气减少到23.2%±21.2。卡巴胆碱引起的I和E细胞放电峰值的变化在数量上是相似的，并且与膈神经活动峰值的变化呈正相关。对这种相关性的分析表明，即使VRG细胞的平均活动保持不变，卡巴胆碱也会在一定程度上抑制膈和肋间活动。此外，我们的数据显示，在卡巴胆碱诱导的呼吸运动神经元抑制过程中，VRG细胞可能接受抑制性和兴奋性输入的组合。因此，尽管可能会发生VRG细胞的一些障碍，但必须有额外的抑制或障碍途径来调节伴随着REM睡眠样张力的隔膜和肋间运动神经元活性的降低。
The microinjection of carbachol into the pons of acute decerebrate cats elicits a REM sleep-like atonia and a profound suppression of respiratory motoneuronal activity (J. Appl. Physiol., 69 (1990) 2280–2289). To assess whether this suppression is mediated by medullary neurons that provide respiratory drive to motoneurons of the respiratory pump muscles (diaphragm and intercostals), we studied the effect of pontine carbachol on the activity of neurons of the ventral respiratory group (VRG) in decerebrate, vagotomized, paralyzed and artificially ventilated cats. VRG neurons were recorded extracellularly along with the activity of phrenic and intercostal (external and internal) nerves. Both inspiratory (I) and expiratory (E) VRG neurons had incrementing, ramp-like bursts of activity during their firing periods and were not vagal motoneurons. Carbachol produced a depression of the peak firing rate in most (42/57) neurons studied. However, five cells showed no change and ten had an increase in activity in spite of consistent depression at the motoneuronal level. For the total population of cells (34 I and 23 E), the peak firing was reduced to 88.5% ± 16.3 (S.D.) of control. The simultaneously recorded phrenic activity was reduced to 77.9% ± 11.5, while inspiratory intercostal activity fell to 63.4% ± 21.6 and expiratory to 23.2% ± 21.2 of control. The carbachol-induced changes in peak firing of both I and E cells were quantitively similar, and positively correlated to changes in peak phrenic activity. Analysis of this correlation suggested that phrenic and intercostal activities will be depressed to some degree by carbachol even when the average VRG cell activity remains unchanged. In addition, our data show that VRG cells may receive a combination of inhibitory and excitatory inputs during the carbachol-induced depression of respiratory motoneurons. Thus, although some disfacilitation from VRG cells may occur, there must be additional inhibitory or disfacilitatory pathways that mediate the decrease in activity of both phrenic and intercostal motoneurons that accompanies the REM sleep-like atonia.