Recent studies have drawn the attention to the link between Alcohol Use Disorder (AUD) and the presence of pain. Indeed, the correct management of pain in patients with a previous history of AUD has been reported to decrease the risk of relapse in alcohol drinking, suggesting that in this prone population, pain may increase the vulnerability to relapse. Previous data in male rats revealed that inflammatory pain desensitizes mu opioid receptors (MORs) in the ventral tegmental area (VTA) and increases intake of high doses of heroine. Due to the relevant role of MORs in alcohol effects, we hypothesize that pain may also alter alcohol reinforcing properties and therefore affect alcohol relapse in male rats. Our microdialysis studies show that the presence of inflammatory pain blunted the increase of extracellular dopamine levels in the Nucleus Accumbens induced by 1.5g/kg of ethanol (s.c.). Moreover, we also revealed that the administration of 52 nmol of ethanol into the VTA failed to induce place preference only in inflammatory pain-suffering animals, and a higher dose (70nmol) was necessary to reverse this effect. Finally, we evaluated the effect of inflammatory pain on the alcohol deprivation effect (ADE) in long-term ethanol-experienced male rats. After four cycles of free ethanol intake and abstinence periods, inflammatory pain induced ADE without affecting its magnitude. These intriguing data reveals the impact of pain on neurochemical and behavioral effects following alcohol administration but also underscore the necessity of finding an appropriate paradigm to determine the long-term behavioral consequences.