Effect of Spinal Gap Junctions in Reduction or Increase of Inflammatory Rat Paw Edema in Presence and Absence of Morphine Usual and Ultra-low Dose

Gap Junctions (G. J) which provide the conduit for cations، second messengers and small metabolites translocation between the neighbor cells are identified in the central nervous system like as spinal cord. As the carbenoxolone is the most frequent blockers of G. J، this study was to investigate the importance of G. J at the level of spinal cord in inflammatory edema induced by formalin merely and at the presence of normal and ultra-low dose of morphine. In this experimental study، 49 male Wistar rats (180-200g) except control group were divided into 7 groups. First، animals were anesthetized and the center of atlas-occipital membrane was undergone surgery to create a small hole for the passage of polyethylene tube. After recovery from cannulation surgery، they were classified in three categories 1) intraperitoneal (i. p) saline، 2) normal dose of morphine (10mg/kg، i. p) 3) ultra-low dose of morphine (1µg/kg، i. p) for intrathecal administration (i. t). Each category was grouped in two groups of seven each (n=7) and one group received saline (i. t) and the second one received carbenoxolone (1nM، i. t). Inflammatory edema volume due to the sub plantar injection of formalin (0. 05 ml، 2. 5%) was assessed in all groups by using plethysmometric method one hour after administration. I. t injection of carbenoxolone reduced the inflammatory edema induced formalin (260±7. 24) (p<0. 001)، also in one hand، potentiated the anti-inflammatory effects of morphine usual dose (220±20. 12) (p<0. 001) and on the other hand، alleviated and reversed the pro-inflammatory effects of morphine ultra-low dose (250±19. 57) (p<0. 001). The results of this study showed that the G. J had an important role in the inflammatory process probably with facilitating the release of inflammatory factors from spinal glia cells. Therefore، G. J blockage possibly diminished the translocation and release of inflammatory mediators through the spinal cord and then leaded to alleviate the inflammatory edema progression and changed the anti-inflammatory/pro-inflammatory effects of morphine.