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Interaction of cannabinoid receptor 2 and social environment modulates chronic alcohol consumption

机译:大麻素受体2与社会环境的相互作用调节慢性饮酒

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摘要

Genetic and environmental factors contribute nearly in equal power to the development of alcoholism. Environmental factors, such as negative life events or emotionally disruptive conditions, initiate and promote alcohol drinking and relapse. The endocannabinoid system is involved in hedonic control and modulates stress reactivity. Furthermore, chronic alcohol drinking alters endocannabinoid signalling, which in turn influences the stress reactivity. Recently, it has been shown that CB2 receptor activity influences stress sensitivity and alcohol drinking. We hypothesized that CB2 receptors influence the impact of environmental risk factors on alcohol preference and consumption. Therefore, in this study, we investigated the alcohol-drinking pattern of wild-type and CB2-deficient animals under single- and group-housing conditions using different alcohol-drinking models, such as forced drinking, intermittent forced drinking and two-bottle choice paradigms. Our data showed that CB2 receptor modulates alcohol consumption and reward. Interestingly, we detected that lack of CB2 receptors led to increased alcohol drinking in the intermittent forced drinking paradigm under group-housing conditions. Furthermore, we found that CB2 knockout mice consumed more food and that their body weight gain was modulated by social environment.
机译:遗传和环境因素几乎对酒精中毒的发展起着相等的作用。环境因素,例如负面的生活事件或情绪破坏性状况,会引发并促进饮酒和复发。大麻素系统参与享乐控制并调节应激反应性。此外,长期饮酒会改变内源性大麻素信号,进而影响应激反应性。最近,已经表明CB2受体活性影响应激敏感性和饮酒。我们假设CB2受体影响环境危险因素对酒精偏好和消费的影响。因此,在这项研究中,我们使用不同的饮酒模式,例如强制性饮酒,间歇性强制性饮酒和两瓶选择,研究了在单居和成群居住条件下野生型和CB2缺乏动物的饮酒模式。范例。我们的数据表明,CB2受体调节酒精消耗和报酬。有趣的是,我们发现缺乏CB2受体会导致在团体居住条件下的间歇性强迫饮酒范例中饮酒增加。此外,我们发现CB2基因敲除小鼠消耗了更多的食物,并且他们的体重增加受到社交环境的调节。

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