Responses of distinct types of sympathetic neuron to stimulation of the superior laryngeal nerve in the cat

Abstract

Stimulation of afferents in the superior laryngeal nerve (SLN) leads to apnea and evokes reflexes in sympathetic neurons. It is not clear whether these reflexes are secondary to changes in the brainstem respiratory network or due directly to the afferent input on neurons belonging to central sympathetic pathways. To clarify this question, single thoracic preganglionic sympathetic neurons projecting into the cervical sympathetic trunk (CST) were classified as described previously and then tested for their responses to electrical stimulation of the superior laryngeal nerve (SLN) in chloralose-anesthetized, paralysed and artificially ventilated cats. SLN stimulation was performed with intensities sufficient to suppress central inspiratory activity detected by phrenic and recurrent laryngeal nerve recordings. Sympathetic neurons were tested under different levels of respiratory drive. Thirteen group I (putative muscle vasoconstrictor) neurons were mostly activated by SLN stimulation when respiratory drive was low, but depressed when it was high; this was due to the change in inspiration-related activity. Ten of eleven group II (putative cutaneous vasoconstrictor) neurons were depressed during SLN stimulation. This inhibition was independent of central respiratory drive. Inhibition also occurred in those neurons which predominantly discharged during postinspiration. Eight group III neurons which showed a discharge confined to inspiration were inhibited but mostly not silenced by SLN stimulation. Group IV (functionally unclassified) neurons either showed no response ( n=5) or were slightly inhibited ( n=2). The responses of group I neurons, but not the responses of group II and group III neurons, showed a significant positive correlation with those of systemic blood pressure. The observed responses corroborate the classification made previously. The results also demonstrate that the responses of sympathetic neurons to SLN stimulation are not merely due to the respiratory modulation of their activity, but rather consist of two components, one occurring independently of and the other secondary to, the changes in respiration.