title: Contribution of peripheral 5-HT2A or 5-HT3 receptors to Fos expression in the trigeminal spinal nucleus produced by acute injury to the masseter muscle during persistent temporomandibular joint inflammation in rats.
abstract: We investigated the contribution of peripheral 5-HT2A or 5-HT3 receptors to Fos expression in the trigeminal spinal nucleus (VSP) following acute masseter muscle injury in male rats with or without temporomandibular joint (TMJ) inflammation persisting for 7 days. TMJ inflammation was evoked by an injection of complete Freund's adjuvant (CFA). Two hours after formalin injection into the masseter muscle produced Fos-like immunoreactivity (Fos-LI) in several regions of the VSP and upper cervical spinal cord (C2), such as ventrolateral (vl) area of the trigeminal subnucleus caudalis (Vc)/subnucleus interpolaris (Vi) transition (vl-Vi/Vc), paratrigeminal nucleus (dPa5), middle portion of the Vc (mid-Vc) and Vc/C2 transition (Vc/C2) regions in both groups. Significant increases in the number of Fos-LI were observed in these areas in CFA group compared with non-CFA group. TMJ inflammation alone did not induce a significant level of Fos-LI in the VSP. In order to assess the effect of antagonizing 5-HT2A or 5-HT3 receptors on formalin-induced Fos-LI, rats were pre-treated with local (masseter muscle) administration of ketanserin or tropisetron (0.01, 0.1 mg/rat) 20 min prior to formalin injection. In CFA group, these antagonists given locally reduced the Fos-LI response in the laminae I-II at the mid-Vc and Vc/C2 regions. These antagonists reduced the Fos-LI response in the dPa5, but not in the vl-Vi/Vc region. The Fos-LI response was not affected by i.v. administration of ketanserin (0.01, 0.1 mg/rat) or tropisetron (0.01 mg/rat). In non-CFA group, these antagonists given locally did not reduce the Fos-LI response. These results suggest that peripheral 5-HT2A and 5-HT3 receptors contribute to nociceptive processing in the masseter muscle in TMJ inflammatory conditions.
authors.affiliation: Department of Physiology, Wakayama Medical University, Wakayama City 641-8509, Japan. jubedog@aol.com
authors.forename: K
authors.initials: K
authors.lastname: Okamoto
authors.forename: A
authors.initials: A
authors.lastname: Kimura
authors.forename: T
authors.initials: T
authors.lastname: Donishi
authors.forename: H
authors.initials: H
authors.lastname: Imbe
authors.forename: Y
authors.initials: Y
authors.lastname: Nishie
authors.forename: H
authors.initials: H
authors.lastname: Matsushita
authors.forename: Y
authors.initials: Y
authors.lastname: Tamai
authors.forename: E
authors.initials: E
authors.lastname: Senba
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005557:Formaldehyde / Q000494:pharmacology; D005620:Freund's Adjuvant / Q000009:adverse effects; D007839:Functional Laterality; D015870:Gene Expression / Q000187:drug effects / Q000502:physiology; D007150:Immunohistochemistry / Q000379:methods; D007211:Indoles / Q000494:pharmacology; D007650:Ketanserin / Q000494:pharmacology; D008297:Male; D008406:Masseter Muscle / Q000293:injuries*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D044402:Receptor, Serotonin, 5-HT2A / Q000502:physiology*; D044406:Receptors, Serotonin, 5-HT3 / Q000378:metabolism*; D012702:Serotonin Antagonists / Q000494:pharmacology; D013705:Temporomandibular Joint Disorders / Q000150:complications / Q000209:etiology / Q000473:pathology*; D014278:Trigeminal Nuclei / Q000378:metabolism*; D000077526:Tropisetron
chemical_list: D007211:Indoles; D016760:Proto-Oncogene Proteins c-fos; D044402:Receptor, Serotonin, 5-HT2A; D044406:Receptors, Serotonin, 5-HT3; D012702:Serotonin Antagonists; D005557:Formaldehyde; D000077526:Tropisetron; D005620:Freund's Adjuvant; D007650:Ketanserin