SOMATOSENSORY SYSTEMS, PAINActivation of trigeminal nociceptive neurons by parotid PAR-2 activation in ratsKawabata, Atsufumi1 CA; Itoh, Hideki1; Kawao, Naoyuki1; Kuroda, Ryotaro1; Sekiguchi, Fumiko1; Masuko, Takashi1; Iwata, Koichi2; Ogawa, Akiko3Author Information 1Division of Physiology and Pathophysiology, and Cell Biology, School of Pharmaceutical Sciences, Kinki University, 3-4-1 Kowakae, Higashi-Osaka 577-8502 2Department of Physiology, Nihon University, School of Dentistry, Tokyo 101-8310 3Department of Dental Anesthesiology, Osaka University Graduate School, Faculty of Dentistry, Suita 565-0871, Japan CACorresponding Author: firstname.lastname@example.org Received 18 March 2004; accepted 19 May 2004 NeuroReport: July 19th, 2004 - Volume 15 - Issue 10 - p 1617-1621 doi: 10.1097/01.wnr.0000134991.97051.6b Buy SDC Metrics Abstract To clarify involvement of protease-activated receptor-2 (PAR-2) in parotid pain, we examined whether PAR-2 activation in the parotid gland could activate trigeminal nociceptive neurons in anesthetized rats, by analyzing immunoreactive Fos as a nociceptive marker. Either the PAR-2 agonist SLIGRL-NH2 or capsaicin, injected into the parotid duct, caused expression of Fos in the trigeminal subnucleus caudalis, although the PAR-2-inactive reversed peptide had no such effect. The Fos expression caused by PAR-2 activation was inhibited by ablation of capsaicin-sensitive sensory neurons. Intraductal SLIGRL-NH2 did not increase vascular permeability in the parotid gland. Our data thus reveal that activation of PAR-2 in the parotid gland can cause activation of trigeminal nociceptive neurons via capsaicin-sensitive sensory nerves most probably by a non-inflammatory mechanism. © 2004 Lippincott Williams & Wilkins, Inc.