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Original Article

Neuropeptide Y in the Rabbit Maxillary Sinus Modulates Cholinergic Acceleration of Mucociliary Activity

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Pages 872-881 | Received 13 Jun 1991, Accepted 07 Apr 1992, Published online: 08 Jul 2009
 

Abstract

The distribution of neuropeptide Y (NPY)-immunoreactivity was investigated in the rabbit maxillary sinus and adjacent ganglia. A moderate supply of NPY-containing nerve fibers occurred around seromucous glands and a denser supply around small blood vessels. Only a few immunoreactive nerve fibers were seen beneath the epithelium. Double immunostain-ing showed that vasoactive intestinal peptide (VIP) coexisted with NPY in the nerve fibers surrounding blood vessels and seromucous glands. NPY-containing nerve cell bodies were numerous in the superior cervical ganglion, and moderately numerous in the sphenopalatine ganglion. The finding of NPY-containing neurons in the latter parasympathetic ganglion suggests that NPY may influence the cholinergic regulation of mucociliary activity. The effect of NPY on the mucociliary activity of the maxillary sinus in connection with cholinergic stimulation has therefore been investigated in vivo using a photoelectric technique. At dosages of 2.5 and 5.0 μg/kg, the ganglionic stimulant nicotine bitartrate, which increases mucociliary activity by a cholinergic pathway, accelerated mucociliary activity by 28.0 ± 7.5% and 36.8 ± 6.2%, respectively. In the same experiment repeated during infusion of NPY (0.1 μg/kg/min), the increase in mucociliary activity was reduced to 10.8 ± 2.3% and 28.9 ± 7.1 %, respectively. Infusion of NPY did not affect the stimulating effect on mucociliary activity by bolus injections (0.1 and 0.5μg/kg) of the cholinergic agonist, methacholine. It is concluded that NPY-like immunoreactivity is present in nerve fibers in the rabbit maxillary sinus and in neurons in the sympathetic and parasympathetic ganglia that supply the nose and paranasal sinuses. NPY attenuates the effect of nicotine on mucociliary activity, probably via a prejunctional mechanism, and may act as a modulator of cholinergic regulation of the mucociliary system.

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