Blockade of D1/D2 dopamine receptors within the nucleus accumbens attenuated the antinociceptive effect of cannabinoid receptor agonist in the basolateral amygdala.

Abstract

Previous studies showed the role of basolateral amygdala (BLA) in cannabinoid-induced antinociception. Furthermore, the nucleus accumbens (NAc) plays an important role in mediating the suppression of pain in animal models. The present study extended the role of dopamine receptors within the NAc in antinociceptive effect of cannabinoid receptor agonist, WIN55,212-2, microinjected into the BLA following the tail-flick and formalin tests in rats. In this study, 174 adult male albino Wistar rats were unilaterally implanted by two separate cannulae into the BLA and NAc. In two separated groups, rats received intra-NAc infusions of the D1 receptor antagonist, SCH-23390 (0.25, 1 and 4 μg/0.5 μl saline) or D2 receptor antagonist, sulpiride (0.25, 1 and 4 μg/0.5 DMSO), and just 2 min later, WIN55,212-2 (15 μg/rat) was microinjected into the BLA. In the tail-flick test, antinociceptive responses of drugs represented as maximal possible effect (%MPE) in 5, 15, 30, 45 and 60min after their administrations. Moreover, in the formalin test, pain related behaviors were monitored in 5-min blocks for 60 min test period. Our findings showed that intra-accumbal SCH-233909 dose-dependently prevented antinociception induced by intra-BLA administration of WIN55,212-2 (15 μg/rat) in time set intervals in formalin, but not tail-flick test. Besides, administration of sulpiride in the NAc could affect WIN-induced analgesia in both models of pain. In conclusion, it seems that D2 receptors located in the NAc, in part, mediate the antinociceptive responses of cannabinoid within the BLA, while D1 receptors only are involved in modulation of persistent inflammatory model of pain.