title: The effect of fentanyl on c-fos expression in the trigeminal brainstem complex produced by pulpal heat stimulation in the ferret.
abstract: 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 fibers originating from the maxillary canine. This study evaluated the effects of the mu-opioid receptor agonist fentanyl on Fos expression evoked by noxious thermal stimulation of the right maxillary and mandibular canines in pentobarbital/chloral hydrate anesthetized adult male ferrets. Pulpal heating evoked Fos expression in two distinct regions of the spinal trigeminal nuclear complex: the transitional region between subnucleus interpolaris and caudalis (Vi/Vc) and within the subnucleus caudalis (Vc). More Fos positive cells were expressed in both regions ipsilateral to the site of stimulation compared with the contralateral side (P < 0.05, ANOVA). Pretreatment with fentanyl significantly and dose-dependently suppressed the number of Fos positive cells in both the Vi/Vc transitional region and Vc (P < 0.05, ANOVA). The suppressive effect of fentanyl on Fos expression was blocked by the 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 failed 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 stimulation is controlled by a naloxone sensitive endogenous opioid system as indicated by Fos expression. Collectively, these results suggest that neuronal populations in Vi/Vc and Vc regions may contribute to pain responses to noxious dental stimulation and these responses can be modulated by both endogenous and exogenous opioids.
authors.affiliation: Dental Research Center, Room 109, University of North Carolina, Chapel Hill, NC 27599-7455, USA Department of Cell and Molecular Physiology, UNC-Chapel Hill, Chapel Hill, NC 27599-7455, USA Institution of Dentistry, University of Turku, Turku, Finland.
authors.forename: Siriporn C
authors.initials: SC
authors.lastname: Chattipakorn
authors.forename: Alan R
authors.initials: AR
authors.lastname: Light
authors.forename: Helen H
authors.initials: HH
authors.lastname: Willcockson
authors.forename: Matti
authors.initials: M
authors.lastname: Närhi
authors.forename: William
authors.initials: W
authors.lastname: Maixner
mesh_terms: D000701:Analgesics, Opioid / Q000494:pharmacology*; D000818:Animals; D001933:Brain Stem / Q000187:drug effects; D003782:Dental Pulp / Q000294:innervation*; D005283:Fentanyl / Q000494:pharmacology; D005289:Ferrets; D006358:Hot Temperature; D007150:Immunohistochemistry; D008297:Male; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D010812:Physical Stimulation; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D017450:Receptors, Opioid, mu / Q000819:agonists*; D014277:Trigeminal Neuralgia / Q000188:drug therapy*; D014279:Trigeminal Nucleus, Spinal / Q000187:drug effects
chemical_list: D000701:Analgesics, Opioid; D009419:Nerve Tissue Proteins; D016760:Proto-Oncogene Proteins c-fos; D017450:Receptors, Opioid, mu; D005283:Fentanyl