Antinociceptive effect of bupropion on visceral pain and its mechanism of action

Abstract

PPurpose: Bupropion is an antidepressant that inhibits noradrenaline and dopamine reuptake. In the current scientific literature, there is limited information regarding the effects of bupropion on pain, predominantly derived from somatic pain studies. This study aims to investigate the impact of bupropion for the first time in visceral pain induced by colorectal distension, a pure visceral pain model, and to reveal the role of various receptors involved in pain control in this effect. Materials and Methods: Male Sprague-Dawley rats were used in the study. Visceral pain was assessed by colorectal distension-induced visceromotor response. Bupropion is administered gastrically at 5, 10, 20, and 40 mg/kg doses. The mechanism of action of bupropion at the spinal cord level was investigated by intrathecal administration of antagonists of α1 and α2 adrenoceptors (prazosin and yohimbine), D1 and D2 dopamine (SCH 23390 and sulpiride) and opioid receptors (naloxone) 10 minutes before bupropion’s effective dose. Results: Bupropion showed significant antinociceptive effects at 20 and 40 mg/kg intragastric doses; no difference was found between these two doses. Intrathecally administered yohimbine (30 µg/rats), sulpiride (30 µg/rats, i.t.), and naloxone (2.5 µg/rats) diminished the antinociceptive effect of bupropion. Prazosin and SCH 23390 did not alter bupropion’s effect. Conclusion: The findings show the antinociceptive effect of bupropion in visceral pain, and adrenergic, dopaminergic, and opioidergic receptors in the spinal cord play a role in this effect.