COUGH-RELATED NEURONS IN THE NUCLEUS TRACTUS SOLITARIUS OF DECEREBRATE CATS

This study was carried out on decerebrate, paralyzed and artificially ventilated cats to investigate the central regulatory mechanism for cough reflex. Fictive cough was induced by repetitive stimulation of the superior laryngeal nerve (SLN) or the nucleus tractus solitarius (NTS), and characterized by an increased inspiratory discharge in the phrenic nerve (stage 1 of cough; SIC) and large burst discharge in the iliohypogastric nerve (stage 2 of cough; S2C). Membrane potential was recorded from the neurons located in the cough-inducible sites of the NTS. Seven augmenting inspiratory (aug-I), 25 inspiratory-modulated (I-mod) and 16 non-respiratory (non-R) neurons were encountered, all of which showed short-latency (7.5 +/- 1.6 ms, n = 48) waves of excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) in response to single pulse stimulation of the SLN. Out of these, all 7 aug-I and 12 I-mod neurons depolarized during the SIC and hyperpolarized during the S2C (DH-type response). Three l-mod and five non-R neurons showed membrane hyperpolarization during both stages (HH-type response). Ten I-mod and three non-R neurons displayed membrane depolarization during the SIC and S2C (DD-type response). The remaining eight non-R neurons showed no response during the fictive cough (NN-type response) but a long-lasting EPSP wave to single SLN stimulation. The NTS neurons recorded here were divided into three groups. Group I neurons with the NN-type response may be the second-order relay neurons. Group II neurons with the DD-type response may integrate the tussigenic afferent information and send a gate signal to the cough pattern generator. Group III neurons with either DH-type or HH-type response may constitute the network of cough pattern generation or modulatory circuits recruited during the cough reflex. The present study suggests that Group II neurons may play a gating role in generating the cough reflex. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.