摘要

Central neuronal interactions may contribute to up regulation of cough in subjects with rhinitis. Previously we have shown that noxious stimulation of the nose induces considerable Fos-like immunoreactivity (FLI) in the solitary nuclei and the region of ventral respiratory group and these neurons are involved in the cough pattern generator. Recent study addressed the question, which additional groups are activated in model of trigeminal hyperresponsiveness and whether some of them might also cooperate with cough pattern gating areas. 24 guinea pigs were sensitized with intraperitoneal ovalbumin (OVA) and later were once weekly challenged with intranasal OVA to develop the neural hyperresponsiveness, 12 animals were left unsensitized. The nasal symptom score was evaluated after each challenge. Finally, animals were anaesthetized and the latest challenges with nasal OVA, capsaicin and saline were applied to induce c-Fos expression in designed groups. Following the survival time animals were deeply anaesthetized, exsanguinated, and transcardially perfused with heparinised saline (200 ml) and paraformaldehyde fixation (200 ml). The brainstems were removed, postfixed, and brainstem slices were processed immunohistochemically (c-Fos, Calbiochem, SR). FLI at the level of obex and areas relative to the obex was analyzed. In all groups (excluding the saline group) the FLI was detected bilaterally in the trigeminal complex, nuclei of solitary tract, lateral reticular and nucleus ambiguus. There were no differences between the OVA and capsaicin groups. Count of Fos-positive neurons within the trigeminal complex does not correlate with the magnitude of clinical symptoms, which gradually increased each week in OVA induced model of hyperresponsiveness. Whereas trigeminal hyperresponsiveness contributes to the up-regulation of cough in animal models, it does not induce any additional neuronal FLI at the middle medulla than observed in naive animals.

  • 出版日期2011-10