ArticlesThe effect of fentanyl onc-fosexpression in the trigeminal brainstem complex produced by pulpal heat stimulation in the ferretChattipakorn, Siriporn C.a,*; Light, Alan R.b; Willcockson, Helen H.b; Närhi, Mattic; Maixner, WilliamaAuthor Information aDental Research Center, Room 109, University of North Carolina, Chapel Hill, NC 27599-7455, USA bDepartment of Cell and Molecular Physiology, UNC-Chapel Hill, Chapel Hill, NC 27599-7455, USA cInstitution of Dentistry, University of Turku, Turku, Finland * Corresponding author. c/o Dr William Maixner. Tel.: +1-919-966-3756; fax: +1-919-966-3683 E-mail address:[email protected] Received October 29, 1998; received in revised form January 22, 1999; accepted February 24, 1999 Pain: August 1, 1999 - Volume 82 - Issue 2 - p 207-215 doi: 10.1016/S0304-3959(99)00046-9 Buy Metrics Abstract We have previously shown that Fos-like immunoreactivity (Fos-LI) is evoked in the brainstem of ferrets following stimulation of pulpal Aδ and C fibers originating from the maxillary canine. This study evaluated the effects of the μ-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. © 1999 Lippincott Williams & Wilkins, Inc.