Oxytocin (OXT) modulates social interactions, attenuates stressful responses and can decrease drug-seeking and taking behaviors. In previous studies, we observed that social defeat (SD) induced a long-lasting increase in ethanol intake and neuroinflammation in male mice. We also know that OXT blocks the increase in cocaine reward induced by SD. Therefore, in the present study we aimed to evaluate the effect of 1 mg/kg of OXT administered 30 min before each episode of SD on ethanol consumption and the neuroinflammatory response in adult male mice. Three weeks after the last SD, mice underwent oral ethanol self-administration (SA) procedure, and striatal levels of the two chemokines CX3CL1 and CXCL12 were measured after the last SD and at the end of the ethanol SA. OXT administration blocked the increase in voluntary ethanol consumption observed in defeated mice, although it did not affect motivation for ethanol. An increase in the striatal levels of CX3CL1 and CXCL12 was observed in defeated animals immediately after the last defeat and after the ethanol SA. However, defeated mice treated with OXT did not show this increase in the neuroinflammatory response. In conclusion, OXT treatment can be a powerful therapeutic target to reduce the negative effects of social stress on ethanol consumption and the neuroinflammatory process.

催产素（OXT）调节社交互动，减轻压力反应，并可以减少寻求药物和采取药物的行为。在以前的研究中，我们观察到社交失败（SD）导致雄性小鼠乙醇摄入量和神经炎症的持续增加。我们也知道OXT会阻止SD诱导的可卡因报酬的增加。因此，在本研究中，我们旨在评估在每次SD发作前30分钟施用1 mg / kg OXT对成年雄性小鼠乙醇消耗和神经炎症反应的影响。在最后一次SD后三周，对小鼠进行口服乙醇自我施用（SA）程序，并在最后一次SD之后和乙醇SA结束时测量了两种趋化因子CX3CL1和CXCL12的纹状体水平。OXT给药阻止了在失败的小鼠中观察到的自愿性乙醇消耗的增加，尽管它并没有影响乙醇的动机。在最后一次失败后和乙醇SA之后立即在失败的动物中观察到CX3CL1和CXCL12的纹状体水平增加。但是，用OXT处理的失败小鼠在神经炎症反应中并未显示出这种增加。总之，OXT治疗可以成为减少社会压力对乙醇消耗和神经炎症过程的负面影响的有力治疗靶标。用OXT治疗的被击败的小鼠在神经炎症反应中没有显示出这种增加。总之，OXT治疗可以成为减少社会压力对乙醇消耗和神经炎症过程的负面影响的有力治疗靶标。用OXT治疗的被击败的小鼠在神经炎症反应中没有显示出这种增加。总之，OXT治疗可以成为减少社会压力对乙醇消耗和神经炎症过程的负面影响的有力治疗靶标。