Changes in P2X3 receptor expression in the trigeminal ganglion following monoarthritis of the temporomandibular joint in rats.
The pathophysiological mechanisms of orofacial deep-tissue pain is still unclear. Previously, P2X receptors (P2XR) in sensory neurons have been shown to play a role in the signal transduction of cutaneous pain. We investigated the functional significance of P2X3R in relation to orofacial deep-tissue pain caused by monoarthritis of the temporomandibular joint (TMJ). Monoarthritis was induced by the injection of complete Freund's adjuvant (CFA) into the unilateral TMJ of the rat. The pain associated with monoarthritis was assessed by the pressure pain threshold (PPT), which was defined as the amount of pressure required to induce vocalization. Fifteen days after CFA-treatment, changes in PPT were examined after injection of P2XR agonists or antagonists into the TMJ. The number of cells expressing P2X3R in trigeminal ganglia (TG) was investigated by immunohistochemistry. Inflamed TMJ showed a continuous decline in PPT during the experimental period (P<0.001). Injection of alpha,beta-meATP, an agonist of P2X1,3,2/3R, dramatically reduced the bilateral PPTs of both inflamed and non-inflamed TMJs (P<0.01) although beta,gamma-me-l-ATP, a selective agonist of P2X1R, did not. The decreased PPTs of inflamed TMJ were reversed either by PPADS, an antagonist of P2X1,2,3,5,1/5,4/5R, or by TNP-ATP, an antagonist of P2X1,3,2/3,1/5R. Immunohistochemically, the number of P2X3R-positive cells increased in the small cell group in TG (P<0.01), whereas there was no change in medium or large cell groups after the CFA-injection. Retrograde tracing confirmed that TMJ neurons in the TG exhibited P2X3R immunoreactivity. Our results suggested that P2X3R plays an important role in orofacial pressure pain caused by monoarthritis of TMJ.
Shinoda
Masamichi
M
Department of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho Showa-ku, Nagoya 466-8550, Japan.
Ozaki
Noriyuki
N
Asai
Hideaki
H
Nagamine
Kenjiro
K
Sugiura
Yasuo
Y
D000255:Adenosine Triphosphate / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D001168:Arthritis / Q000139:chemically induced / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D002452:Cell Count / Q000379:methods; D004347:Drug Interactions; D005157:Facial Pain / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D005620:Freund's Adjuvant / Q000009:adverse effects; D007839:Functional Laterality; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D017288:Pain Threshold / Q000187:drug effects / Q000502:physiology; D058910:Purinergic P2 Receptor Agonists; D058919:Purinergic P2 Receptor Antagonists; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D051381:Rats; D011917:Rats, Inbred Lew; D018048:Receptors, Purinergic P2 / Q000378:metabolism*; D058477:Receptors, Purinergic P2X3; D013266:Stilbamidines / Q000378:metabolism; D013705:Temporomandibular Joint Disorders / Q000139:chemically induced / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D013997:Time Factors; D012668:Trigeminal Ganglion / Q000166:cytology / Q000378:metabolism* / Q000503:physiopathology
C049774:2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; C546410:P2rx3 protein, rat; D058910:Purinergic P2 Receptor Agonists; D058919:Purinergic P2 Receptor Antagonists; D018048:Receptors, Purinergic P2; D058477:Receptors, Purinergic P2X3; D013266:Stilbamidines; C077792:pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid; C005147:5'-adenylyl (beta,gamma-methylene)diphosphonate; D011732:Pyridoxal Phosphate; C045674:2',3'-O-(2,4,6-trinitro-cyclohexadienylidine)adenosine 5'-triphosphate; D000255:Adenosine Triphosphate; D005620:Freund's Adjuvant; C002630:alpha,beta-methyleneadenosine 5'-triphosphate