Central cyclooxygenase inhibitors reduced IL-1β-induced hyperalgesia in temporomandibular joint of freely moving rats

• Published in: Pain (Amsterdam) Vol. 117; no. 1; pp. 204 - 213
• Main Authors: Ahn, Dong K., Chae, Jong M., Choi, Hyo S., Kyung, Hee M., Kwon, Oh W., Park, Hyo S., Youn, Dong H., Bae, Yong C.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 01.09.2005; Elsevier
• Subjects: Biological and medical sciences; Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction; Cyclooxygenase inhibitor; Formalin; Hyperalgesia; IL-1β; Medical sciences; Nervous system (semeiology, syndromes); Nervous system as a whole; Neurology; TMJ; TMJ; Formalin; IL-1β; Cyclooxygenase inhibitor; Hyperalgesia; Rat; 1L-1β; Cytokine; Rodentia; Temporomandibular joint; Hand; Osteoarticular system; Vertebrata; Paracetamol; Mammalia; Pain; Microinjection; Treatment; Interleukin 1; Models; Behavior; Biological receptor
• ISSN: 0304-3959; 1872-6623
• DOI: 10.1016/j.pain.2005.06.009

Microinjection of formalin (5%, 50 μl) into a temporomandibular joint (TMJ) causes noxious behavioral responses in freely moving rats. In the present study, we investigated the role of central cyclooxygenase (COX) pathways in IL-1β-induced hyperalgesia with formalin-induced TMJ pain model. Intra-articular injection of 100 pg or 1 ng of IL-1β significantly facilitated formalin-induced behavior by 130 or 174% in the number of scratches. Intracisternal administration of 100 pg or 1 ng of IL-1β also significantly increased formalin-induced behavior by 166 or 82% in the number of scratches. IL-1β-induced hyperalgesia was blocked by pretreatment with IL-1 receptor antagonist. Intracisternal pretreatment with SC-560, a selective COX-1 inhibitor, or NS-398, a selective COX-2 inhibitor, abolished intra-articular administration of IL-1β-induced hyperalgesic response. Intracisternal pretreatment with NS-398, a selective COX-2 inhibitor, abolished the intracisternal administration of IL-1β-induced hyperalgesic response, while pretreatment with SC-560, a selective COX-1 inhibitor, did not change IL-1β-induced hyperalgesic responses. On the other hand, pretreatment with acetaminophen, a tentative COX-3 inhibitor, also abolished both intra-articular and intracisternal administration of IL-1β-induced hyperalgesic responses. These results indicate that central COX-2 plays important role in the central administration of IL-1β-induced hyperalgesia and that central COX-1/2 pathways mediate peripheral administration of IL-1β-induced hyperalgesia in the TMJ. Central COX-3 inhibitor seems to play an important role in the nociceptive process associated with both peripheral and central administration of IL-1β-induced hyperalgesia in TMJ. It is concluded that central acting of COX-3 inhibitors may be of therapeutic value in the treatment of inflammatory pain in TMJ.