Gerber U, Polosa C
Can J Physiol Pharmacol. 1979 Oct;57(10):1073-81. doi: 10.1139/y79-161.
Repetitive electrical stimulation of afferent fibers in the superior laryngeal nerve (SLN) evoked depressant or excitatory effects on sympathetic preganglionic neurons of the cervical trunk in Nembutal-anesthetized, paralyzed, artifically ventilated cats. The depressant effect, which consisted of suppression of the inspiration-synchronous discharge of units with such firing pattern, was obtained at low strength and frequency of stimulation (e.g. 600 mV, 30 Hz) and was absent at end-tidal CO2 values below threshold for phrenic nerve activity. The excitatory effect required higher intensity and frequency of stimulation and was CO2 independent. The depressant effect on sympathetic preganglionic neurons with inspiratory firing pattern seemed a replica of the inspiration-inhibitory effect observed on phrenic motoneurons. Hence, it could be attributed to the known inhibition by the SLN of central inspiratory activity, if it is assumed that this is a common driver for phrenic motoneurons and some sympathetic preganglionic neurons. The excitatory effect, on the other hand, appears to be due to connections of SLN afferents with sympathetic preganglionic neurons, independent of the respiratory center.
在戊巴比妥麻醉、麻痹并人工通气的猫中，对上喉神经（SLN）传入纤维进行重复电刺激，可诱发颈交感神经节前神经元出现抑制或兴奋效应。抑制效应表现为抑制具有这种放电模式的神经元的吸气同步放电，在低强度和低频率刺激（如600 mV，30 Hz）时出现，而在呼气末二氧化碳值低于膈神经活动阈值时则不存在。兴奋效应需要更高的刺激强度和频率，且与二氧化碳无关。对具有吸气放电模式的交感神经节前神经元的抑制效应似乎是在膈运动神经元上观察到的吸气抑制效应的翻版。因此，如果假定这是膈运动神经元和一些交感神经节前神经元的共同驱动因素，那么它可归因于已知的SLN对中枢吸气活动的抑制。另一方面，兴奋效应似乎是由于SLN传入纤维与交感神经节前神经元的连接，与呼吸中枢无关。
