Evidence for the involvement of endogenous ATP and P2X receptors in TMJ pain

Maria Cláudia G Oliveira; Carlos Amílcar Parada; Maria Cecília Ferraz Arruda Veiga; Luciane Rocha Rodrigues; Silvana Pereira Barros; Cláudia Herrera Tambeli

doi:10.1016/j.ejpain.2004.04.006

Evidence for the involvement of endogenous ATP and P2X receptors in TMJ pain

Eur J Pain. 2005 Feb;9(1):87-93. doi: 10.1016/j.ejpain.2004.04.006.

Authors

Maria Cláudia G Oliveira¹, Carlos Amílcar Parada, Maria Cecília Ferraz Arruda Veiga, Luciane Rocha Rodrigues, Silvana Pereira Barros, Cláudia Herrera Tambeli

Affiliation

¹ 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.

PMID: 15629879
DOI: 10.1016/j.ejpain.2004.04.006

Abstract

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.

MeSH terms

Adenosine Triphosphate / analogs & derivatives*
Adenosine Triphosphate / metabolism*
Adenosine Triphosphate / pharmacology
Animals
Anti-Inflammatory Agents / pharmacology
Arthralgia / metabolism*
Arthralgia / physiopathology
Arthritis / chemically induced
Arthritis / metabolism
Arthritis / physiopathology
Carrageenan / antagonists & inhibitors
Disease Models, Animal
Down-Regulation / drug effects
Down-Regulation / physiology
Lidocaine / analogs & derivatives*
Lidocaine / pharmacology
Male
Nociceptors / drug effects
Nociceptors / metabolism*
Purinergic P2 Receptor Agonists
Purinergic P2 Receptor Antagonists
Pyridoxal Phosphate / analogs & derivatives*
Pyridoxal Phosphate / pharmacology
Rats
Rats, Wistar
Receptors, Purinergic P2 / metabolism*
Receptors, Purinergic P2X
Sensory Receptor Cells / metabolism
Sensory Receptor Cells / physiopathology
Temporomandibular Joint / innervation
Temporomandibular Joint / physiopathology*
Temporomandibular Joint Disorders / chemically induced
Temporomandibular Joint Disorders / metabolism*
Temporomandibular Joint Disorders / physiopathology

Substances

Anti-Inflammatory Agents
Purinergic P2 Receptor Agonists
Purinergic P2 Receptor Antagonists
Receptors, Purinergic P2
Receptors, Purinergic P2X
pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid
QX-314
Pyridoxal Phosphate
Adenosine Triphosphate
Carrageenan
Lidocaine
alpha,beta-methyleneadenosine 5'-triphosphate