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首页> 外文期刊>Addiction biology >Evidence that vasopressin V 1b receptors mediate the transition to excessive drinking in ethanol-dependent rats
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Evidence that vasopressin V 1b receptors mediate the transition to excessive drinking in ethanol-dependent rats

机译：血管加压素V 1b受体介导乙醇依赖性大鼠过度饮酒的证据

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Alcoholism is a devastating condition that represents a progression from initial alcohol use to dependence. Although most individuals are capable of consuming alcohol in a limited fashion, the development of alcohol dependence in a subset of individuals is often associated with negative emotional states (including anxiety and depression). Since the alleviation of this negative motivational state via excessive alcohol consumption often becomes a central goal of alcoholics, the transition from initial use to dependence is postulated to be associated with a transition from positive to negative reinforcement mechanisms. Vasopressin is a neuropeptide known to potentiate the effects of CRF on the HPA axis, and emerging evidence also suggests a role for centrally located vasopressin acting on V 1b receptors in the regulation of stress- and anxiety-like behaviors in rodents. The present study determined state-dependent alterations in vasopressin/V 1bR signaling in an animal model of ethanol dependence. The V 1bR antagonist SSR149415 dose-dependently reduced excessive levels of ethanol self-administration observed in dependent animals without affecting the limited levels of ethanol drinking in non-dependent animals. Ethanol self-administration reduced V 1b receptor levels in the basolateral amygdala of non-dependent animals, a neuroadaptation that could theoretically facilitate the positive reinforcing effects of alcohol. In contrast, V 1bR levels were seemingly restored in ethanol-dependent rats, a switch that may in part underlie a transition from positive to negative reinforcement mechanisms with dependence. Together, our data suggest a key role for vasopressin/V 1bR signaling in the transition to ethanol dependence.
机译：酒精中毒是一种破坏性疾病，代表了从最初的饮酒到依赖的发展。尽管大多数人都有能力以有限的方式饮酒，但是一部分人对酒精的依赖往往与不良的情绪状态（包括焦虑和抑郁）相关。由于通过过量饮酒来缓解这种消极的动机状态通常成为酗酒者的主要目标，因此假定从最初使用到依赖的过渡与从积极强化机制向消极强化机制的转化相关。血管加压素是一种已知的神经肽，可增强CRF对HPA轴的作用，新出现的证据也表明，位于血管中的加压素对V 1b受体的作用可能在啮齿动物的应激和焦虑样行为的调节中发挥作用。本研究确定了乙醇依赖性动物模型中加压素/ V 1bR信号传导的状态依赖性改变。 V 1bR拮抗剂SSR149415剂量依赖性地降低了在依赖动物中观察到的过量乙醇自我管理水平，而不影响非依赖动物中有限的乙醇饮用水平。乙醇的自我给药降低了非依赖性动物基底外侧杏仁核中的V 1b受体水平，这是一种神经适应，理论上可以促进酒精的积极增强作用。相反，在乙醇依赖的大鼠中，V 1bR水平似乎得以恢复，这一转变可能部分是由依赖引起的从正向增强机制向负向增强机制转变的基础。在一起，我们的数据表明血管加压素/ V 1bR信号转导到乙醇依赖过渡中的关键作用。

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