Papel periférico e central dos receptores P2X7 nos mecanismos de dor nociceptiva na atm de ratos

Abstract

Nociceptive pain in the temporomandibular joint (TMJ) is present in many clinical conditions. P2X7 receptors are involved in TMJ nociception, however the mechanism that involves these receptors in the pathophysiology of inflammatory TMJ pain is still uncle ar. The objective of the present work was to study the role of P2X7 receptors in the mechanisms of nociceptive pain in the TMJ of rats. The experimental protocol was approved by CEUA-UFC Campus Sobral (14/2020). 40 animals (n=5) were pre-treated (i .p) with saline (0,9%) or Brilliant Blue G (50 mg/kg), selective P2X7 receptor antagonist, or indomethacin (5mg/kg), non-steroidal anti-inflammatory drug. -steroidal. After 1h, an intra-articular (I.A) injection of saline (50 uL, 0,9%) or formalin (50 uL,1,5%) was applied in the left TMJ, after a brief (30s) anesthesia with isoflurane (3%). Nociceptive behavior was assessed for 45 min. Immediately after the behavioral analyses, the rats were anesthetized with ketamine:xylazine (90:10 mg/kg, i.p). After euthanasia, the trigeminal ganglion (GT) and caudal subnucleus (SC) were removed for analysis of the expression of mRNA levels of P2X7 receptors and cytokines TNF-, IL-1 and IL-6 by q-RT-PCR. Data were expressed as mean±SEM. Parametric data were analyzed by Analysis of Variance (ANOVA) followed by the Tukey post-test’s multiple comparisons. BBG treatment reduced nociceptive pain (P<0,0001), and expression of the P2X7 receptor gene (P<0,002) and TNF- cytokines and IL-1 (P<0,0001), when compared to the formalin group, both in GT and SC. BBG had a potential antinociceptive effect in blocking P2X7 receptors by reducing gene expression of cytokines in both peripheral and central SN, however, the chronic study of TMJ hypernociception is necessary.