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首页> 外文期刊>Addiction biology >Oxytocin inhibits ethanol consumption and ethanol-induced dopamine release in the nucleus accumbens
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Oxytocin inhibits ethanol consumption and ethanol-induced dopamine release in the nucleus accumbens

机译：催产素抑制乙醇消耗和乙醇诱导的细胞核中的多巴胺释放

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摘要

Alcohol (EtOH) is one of the most widely abused recreational drugs and is arguably the most harmful. However, current treatment options for alcohol-use disorders generally have limited efficacy and poor uptake in the community. In this context, the neuropeptide oxytocin (OXT) has emerged as a promising potential treatment option for a number of substance-use disorders, including alcoholism. The utility of OXT in reducing consumption of and craving for a wide range of substances may lie in its ability to modulate drug-induced neurochemical effects within the mesolimbic dopamine pathway. However, the impact of OXT on EtOH actions in this pathway has yet to be explored. Here, we reveal that an acute intracerebroventricular (icv) infusion of OXT (1 mu g/5 mu l) attenuated voluntary EtOH (20 percent) self-administration after chronic intermittent access to EtOH for 59 days (28 drinking sessions) in male Wistar rats. Next, we demonstrated that an acute intraperitoneal (ip) injection of EtOH (1.5 g/kg, 15 percent w/v) increased dopamine release within the nucleus accumbens in both EtOH-naive rats and rats that had received 10 daily ip injections of EtOH. Icv OXT completely blocked the EtOH-induced dopamine release in both EtOH-naive and chronically treated rats. The attenuation of EtOH-induced dopamine release by OXT may help to explain the reduced EtOH self-administration observed following icv OXT infusion.
机译：酒精（Etoh）是最广泛滥用的休闲药物之一，可以是最有害的。然而，当前的饮酒障碍的治疗方案通常具有有限的疗效和群体的吸收差。在这种情况下，神经肽催产素（OXT）被出现为许多物质使用障碍，包括酗酒的有希望的潜在治疗选择。 OXT在减少各种物质的消费和渴望消费和渴望中的效用可能位于其调节药物诱导的药物诱导的细胞化学途径中的能力。然而，OXT对本途径中ETOH行动的影响尚未探索。在这里，我们揭示了急性脑室（ICV）输注OXT（1μg/5μl）在慢性间歇进入雄性Wistar（28次饮用会议）后慢性间歇性慢性间歇性（28次饮用会话）后的自愿EtOH（20％）自我给药老鼠。接下来，我们证明，注射EtOH（1.5g / kg，15％w / v）的急性腹膜内（Ip）注射细胞核内的多巴胺释放在核心的大鼠和大鼠中，该大鼠均为10个每日IP注射的EtOH 。 ICV OXT完全阻止了EtOH-Naive和慢性处理的大鼠中的EtOH诱导的多巴胺释放。 OXT的EtOH诱导的多巴胺释放的衰减可能有助于解释在ICV OXT输注后观察到的eTOH自我给药。

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