Evidence for the involvement of endogenous ATP and P2X receptors in TMJ pain.
Evidence is accumulating which supports a role for ATP in the initiation of pain by acting on P2X receptors expressed on nociceptive afferent nerve terminals. To investigate whether these receptors play a role in temporomandibular (TMJ) pain, we studied the presence of functional P2X receptors in rat TMJ by examining the nociceptive behavioral response to the application of the selective P2X receptor agonist alpha,beta-methylene ATP (alpha,beta-meATP) into the TMJ region of rat. The involvement of endogenous ATP in the development of TMJ inflammatory hyperalgesia was also determined by evaluating the effect of the general P2 receptor antagonist pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) on carrageenan-induced TMJ inflammatory hyperalgesia. Application of alpha,beta-meATP into the TMJ region of rats produced significant nociceptive responses that were significantly reduced by the co-application of lidocaine N-ethyl bromide quaternary salt, QX-314, (2%) or of the P2 receptor antagonist PPADS. Co-application of PPADS with carrageenan into the TMJ significantly reduced inflammatory hyperalgesia. The results indicate that functional P2X receptors are present in the TMJ and suggest that endogenous ATP may play a role in TMJ inflammatory pain mechanisms possibly by acting primarily in these receptors.
Oliveira
Maria Cláudia G
MC
Laboratory of Orofacial Pain, Department of Physiology, Faculty of Dentistry of Piracicaba, University of Campinas - UNICAMP, Limeira Av, 901 Zip Code, 13414-900, Piracicaba, SP, Brazil.
Parada
Carlos Amílcar
CA
Veiga
Maria Cecília Ferraz Arruda
MC
Rodrigues
Luciane Rocha
LR
Barros
Silvana Pereira
SP
Tambeli
Cláudia Herrera
CH
D000255:Adenosine Triphosphate / Q000031:analogs & derivatives* / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D018771:Arthralgia / Q000378:metabolism* / Q000503:physiopathology; D001168:Arthritis / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D002351:Carrageenan / Q000037:antagonists & inhibitors; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D008012:Lidocaine / Q000031:analogs & derivatives* / Q000494:pharmacology; D008297:Male; D009619:Nociceptors / Q000187:drug effects / Q000378:metabolism*; D058910:Purinergic P2 Receptor Agonists; D058919:Purinergic P2 Receptor Antagonists; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D018048:Receptors, Purinergic P2 / Q000378:metabolism*; D058469:Receptors, Purinergic P2X; D011984:Sensory Receptor Cells / Q000378:metabolism / Q000503:physiopathology; D013704:Temporomandibular Joint / Q000294:innervation / Q000503:physiopathology*; D013705:Temporomandibular Joint Disorders / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology
D000893:Anti-Inflammatory Agents; D058910:Purinergic P2 Receptor Agonists; D058919:Purinergic P2 Receptor Antagonists; D018048:Receptors, Purinergic P2; D058469:Receptors, Purinergic P2X; C077792:pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid; C012647:QX-314; D011732:Pyridoxal Phosphate; D000255:Adenosine Triphosphate; D002351:Carrageenan; D008012:Lidocaine; C002630:alpha,beta-methyleneadenosine 5'-triphosphate