The effect of fentanyl on c-fos expression in the trigeminal brainstem complex produced by pulpal heat stimulation in the ferret

We have previously shown that Fos-like immunoreactivity (Fos-LI) is evoked in the brainstem of ferrets following stimulation of pulpal A delta and C f ibers originating from the maxillary canine. This study evaluated the effec ts of the mu-opioid receptor agonist fentanyl on Fos expression evoked by n oxious thermal stimulation of the right maxillary and mandibular canines in pentobarbital/chloral hydrate anesthetized adult male ferrets. Pulpal heat ing evoked Fos expression in two distinct regions of the spinal trigeminal nuclear complex: the transitional region between subnucleus interpolaris an d caudalis (Vi/Vc) and within the subnucleus caudalis (Vc). More Fos positi ve cells were expressed in both regions ipsilateral to the site of stimulat ion compared with the contralateral side (P < 0.05, ANOVA). Pretreatment wi th fentanyl significantly and dose-dependently suppressed the number of Fos positive cells in both the Vi/Vc transitional region and Vc (P < 0.05, ANO VA). The suppressive effect of fentanyl on Fos expression was blocked by th e intravenous administration of naloxone, an opioid antagonist, indicating a specific opioid receptor effect. In addition, opioid receptor antagonism with naloxone alone enhanced Fos expression in Vi/Vc and Vc in response to heat stimulation. The administration of naloxone without heat stimulation f ailed to evoke Fos expression in Vi/Vc and Vc. These findings suggest that the activation of trigeminal Vi/Vc and Vc neurons by noxious dental heat st imulation is controlled by a naloxone sensitive endogenous opioid system as indicated by Fos expression. Collectively, these results suggest that neur onal populations in Vi/Vc and Vc regions may contribute to pain responses t o noxious dental stimulation and these responses can be modulated by both e ndogenous and exogenous opioids. (C) 1999 International Association for the Study of Pain. Published by Elsevier Science B.V.