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Abstract: Central neuronal interaction seems to play a role in pathogenesis of upper airway cough syndrome. In the guinea pig model we used the method c-fos expression to identify neurons involved in processing of nociceptive nasal stimuli and their contribution to enhancement of cough. 21 spontaneously breathing, urethane anaesthetized animals were used. The controls received intranasal saline, stimulation group received capsaicin (15μl, 50μM), and not-treated group was free of nasal challenge. After 2h animals were deeply anaesthetized, exsanguinated and transcardially perfused with saline and paraformaldehyde. The brainstems were removed, post-fixed, and slices were processed immunohistochemically for c-fos. In capsaicin group the FLI was detected in the nTs 0.5mm caudal, 1.5mm lateral to the obex, the area postrema, LRN and VRG. Intensive FLI was identified in trigeminal nuclear complex. Mean number of FOS positive neurons per section was significantly higher in capsaicin group than that in no-treatment controls or saline controls at the level of obex (p<0.01). Neurons of nTs and VRG clearly activated after nasal provocation may participate in enhancement of cough. [ABSTRACT FROM AUTHOR]

Highlights • Evidence for complex rostral NTS neuronal structures employed in the control of coughing. • GABA-ergic modulation of number, expiratory efforts and inspiratory timing of cough. • Evidence for limited role of GABA B receptors in the rostral NTS in the control of inspiratory cough efforts. • Limited effect of GABA-ergic neurotransmission in the caudal NTS on cough in cat. • Evidence for significant species differences in the cough circuitry between cats and rabbits. Abstract GABA, muscimol, and baclofen were microinjected into the rostral (rNTS) and caudal solitary tract nucleus (cNTS) in 24 anesthetized cats. Electromyograms (EMGs) of diaphragm (DIA) and abdominal muscles (ABD), blood pressure and esophageal pressure (EP) were recorded and analysed. Bilateral microinjections of 1 mM GABA (total 66 ± 4 nl), 1 mM baclofen (64 ± 4 nl) and unilateral microinjections of 0.5 mM muscimol (33 ± 1 nl) in the rNTS significantly reduced cough number (CN), amplitudes of ABD EMGs, expiratory EP, and prolonged the duration of the cough inspiratory phase. GABA microinjections decreased the amplitudes of cough-related DIA EMGs and inspiratory EP; muscimol microinjections decreased the cough DIA EMG on the contralateral side. Only microinjections of GABA into the cNTS suppressed CN. In some cases, microinjections prolonged the inspiratory phase, lowered respiratory rate, changed the depth of breathing, and increased blood pressure and heart rate. Our results confirm that GABA-ergic inhibitory mechanisms in the rNTS can regulate coughing in the anesthetized cat. [ABSTRACT FROM AUTHOR]

Highlights: [•] We learned very useful lessons from apnoea/hypopnoea and its role in airway defence. [•] Intranasal administration of AITC inhibits coughing in anaesthetized guinea pigs. [•] Intranasal administration of AITC inhibits coughing in conscious guinea pigs. [•] Inhibition of coughing in conscious model is prevented by TRPA1 antagonist AP 18. [Copyright &y& Elsevier]

Abstract: Eighteen healthy volunteers with normal lung function were tested for cough. Before and after nasal administration of thymol (0.025ml, 10−3 M) into both nostrils, urge-to-cough, cough threshold, cumulative and total count of coughs per provocation were estimated during standardized and validated capsaicin cough challenge. Nasal thymol challenges induced pleasant olfactory sensation and in 6 out of the 18 subjects also mild cooling sensation. Cough threshold was not influenced when compared with intranasal saline and vehicle challenges (12.5 vs. 13.2 vs. 10.2μM of capsaicin to induce two or more coughs (C2), respectively), but the total count of coughs after nasal thymol challenge was significantly lower than that obtained after saline or vehicle (19 vs. 20 vs. 14 coughs/provocation, respectively; p <0.05). Importantly, subjects did not report the urge to cough, which appeared to correspond to C2. We conclude that the modulation of cough by thymol is mostly of olfactory origin. [Copyright &y& Elsevier]