Abstract
The peripheral chemoreceptors of the trigeminal system in the nasal cavity are presumed to be free nerve endings arising from Adelta and C fibers. These fibers appear to be scattered throughout the nasal epithelium, and arise from the nasopalatine and ethmoid branches of the trigeminal nerve. In the present study, the effects of nicotinic acetylcholine receptor (nAChR) blockers on ethmoid nerve responses to nicotine and cyclohexanone were examined. Multiunit neural recordings were obtained from the ethmoid nerve of Sprague-Dawley rats. Vapor-phase nicotine (12.5 p.p.m.) and cyclohexanone (450 p.p. m.) were delivered to the rats' nares via an air-dilution olfactometer. The magnitude of the response to nicotine decreased after the administration of the nAChR blockers dihydro-beta-erythroidine hydrobromide (DHBE) and mecamylamine hydrochloride. DHBE is a competitive nicotinic receptor antagonist specific for the alpha4beta2 receptor subtype and mecamylamine is known to bind alpha3beta4 and alpha4beta2 receptors. The nAChR blockers had no effect on ethmoid nerve responses to cyclohexanone. These results suggest that the mechanism by which at least one irritant stimulates nasal trigeminal nerve endings involves the binding of irritant with a specific receptor.
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