Effects of pharyngolaryngeal injury on nociceptive swallowing reflexes

OBJECTIVES: Although pharyngolaryngeal injury impairs water-evoked swallowing, its influence on nociceptive swallowing reflexes remains unclear. Therefore, this study aimed to determine the effects of pharyngolaryngeal injury on nociceptive receptor-dependent swallowing reflexes. METHODS: Adult male rats underwent endoscopic evaluation of swallowing under anesthesia. The number, latency, and swallowing intervals were quantified. Distilled water, capsaicin (TRPV1 agonist), and allyl isothiocyanate (AITC, TRPA1 agonist) were infused onto the pharyngolaryngeal surface via a syringe pump at a constant flow for 10 s. Blue-dyed water confirmed gastric delivery. Pharyngolaryngeal injury was induced by topical application of 10 % acetic acid. The nodose and petrosal/jugular-complex ganglia were analyzed for TRPV1 and TRPA1 gene expression using quantitative RT-PCR. RESULTS: Gastric delivery from the pharyngolaryngeal region was confirmed with blue-dyed water, although aspiration was observed, indicating the reliability of the endoscopic swallowing evaluation. Pharyngolaryngeal injury significantly suppressed water-evoked swallowing, consistent with previous findings. Contrastingly, capsaicin robustly evoked swallowing post-injury, with attenuated desensitization upon repeated stimulation. AITC did not change the number of swallows but prolonged latency. Quantitative RT-PCR revealed significant upregulation of TRPV1 gene expression in the petrosal/jugular-complex ganglia, whereas TRPA1 expression remained unchanged in both ganglia. CONCLUSION: Nociceptive stimuli elicit swallowing via mechanisms that are distinct from those activated by water. Reduced desensitization of capsaicin-evoked swallowing after pharyngolaryngeal injury suggests facilitation through TRPV1-dependent pathways, potentially driven by increased TRPV1 expression in petrosal/jugular-complex afferents.