Central ghrelin inhibits reflex swallowing elicited by activation of the superior laryngeal nerve in the rat.

The effect of ghrelin on rhythmic reflex swallowing was examined in urethane-chloralose anesthetized rats. Swallowing was monitored by recording electromyographic activities of the suprahyoid muscle. Fourth ventricular administration of ghrelin decreased swallowing frequency during electrical stimulation of the central cut end of the superior laryngeal nerve (SLN stimulation). A significant decrease in swallowing frequency was observed after ghrelin administration at doses of 3, 10, 30 and 100 pmol. The administration of ghrelin with growth hormone secretagogue receptor antagonist ([D-Lys(3)] GHRP-6) did not change swallowing frequency during SLN stimulation. Neither mean blood pressure nor heart rate changed after the administration of 10 pmol ghrelin. Bilateral vagotomy did not disrupt the ghrelin response. These observations indicate that the ghrelin response does not depend on either cardiovascular or abdominal responses. Microinjection of ghrelin (0.3 pmol) into the vicinity of the solitary tract inhibited swallowing induced by SLN stimulation. Fourth ventricular administration of orexin-A (3 nmol) also inhibited reflex swallowing elicited by SLN stimulation. These results suggest that ghrelin and other orexigenic peptides inhibit reflex swallowing by modifying neural activities of the dorsal medulla where the swallowing center is housed.

Central neuropeptide Y induces proximal stomach relaxation via Y1 receptors in the dorsal vagal complex of the rat.

Effects of neuropeptide Y (NPY) on motility of the proximal stomach was examined in anesthetized rats. Intragastric pressure was measured using a balloon situated in the proximal part of the stomach. Administration of NPY into the fourth ventricle induced relaxation of the proximal stomach in a dose-dependent manner. Administration of an Y1 receptor (Y1R) agonist [Leu31, Pro34]NPY induced a larger relaxation than NPY. The administration of an Y2 receptor agonist (NPY 13-36) did not induce significant changes in motility. Microinjections of [Leu31, Pro34]NPY into the caudal part of the dorsal vagal complex (DVC) induced relaxation of the proximal stomach. In contrast, similar injections into the intermediate part of the DVC increased IGP of the proximal stomach. Administration of NPY into the fourth ventricle did not induce relaxation after bilateral injections of the Y1R antagonist (1229U91) into the caudal DVC. These results indicate that NPY induces relaxation in the proximal stomach via Y1Rs situated in the DVC. Because bilateral vagotomy below the diaphragm abolished the relaxation induced by the administration of NPY into the fourth ventricle, relaxation induced by NPY is probably mediated by vagal preganglionic neurons. Intravenous injection of atropine methyl nitrate reduced relaxation induced by administration of NPY. Therefore, relaxation induced by NPY is likely mediated by peripheral cholinergic neurons.