Activation of trigeminal nociceptive neurons by parotid PAR-2 activation in rats
Autor: | Takashi Masuko, Akiko Ogawa, Koichi Iwata, Atsufumi Kawabata, Ryotaro Kuroda, Naoyuki Kawao, Fumiko Sekiguchi, Hideki Itoh |
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Rok vydání: | 2004 |
Předmět: |
Male
medicine.medical_specialty Time Factors Cell Count In Vitro Techniques Parotid duct Functional Laterality Trigeminal ganglion stomatognathic system Internal medicine medicine Animals Parotid Gland Receptor PAR-2 Drug Interactions Receptor PAR-1 RNA Messenger Rats Wistar Neurons Medulla Oblongata Reverse Transcriptase Polymerase Chain Reaction Chemistry General Neuroscience Spinal trigeminal nucleus Nociceptors Immunohistochemistry Sensory neuron Rats Parotid gland Oncogene Proteins v-fos medicine.anatomical_structure Endocrinology Trigeminal Ganglion Medulla oblongata Nociceptor Capsaicin Oligopeptides Sensory nerve |
Zdroj: | NeuroReport. 15:1617-1621 |
ISSN: | 0959-4965 |
DOI: | 10.1097/01.wnr.0000134991.97051.6b |
Popis: | 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. |
Databáze: | OpenAIRE |
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