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首页> 外文期刊>Addiction biology >Central administration of the anorexigenic peptide neuromedin U decreases alcohol intake and attenuates alcohol-induced reward in rodents
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Central administration of the anorexigenic peptide neuromedin U decreases alcohol intake and attenuates alcohol-induced reward in rodents

机译：厌氧肽的中央疗法uGeuredin U降低酒精摄入并在啮齿动物中衰减酒精诱导的奖励

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摘要

By investigating the neurochemical mechanisms through which alcohol activates the brain reward systems, novel treatment strategies for alcohol use disorder (AUD), a chronic relapsing disease, can be developed. In contrast to the common view of the function of gut-brain peptides, such as neuromedin U (NMU), to regulate food intake and appetite, a novel role in reinforcement mediation has been implied. The anorexigenic effects of NMU are mediated via NMU2 receptors, preferably in the arcuate nucleus and paraventricular nucleus. The expression of NMU2 receptors is also expressed in several reward-related areas in the brain, suggesting a role in reward regulation. The present experiments were therefore set up to investigate the effect of intracerebroventricular administration of NMU on alcohol-mediated behaviors in rodents. We found that central administration of NMU attenuated alcohol-induced locomotor stimulation, accumbal dopamine release and the expression of conditioned place preference in mice. In addition, NMU dose dependently decreased alcohol intake in high, but not in low, alcohol-consuming rats. Central NMU administration did not alter the blood alcohol concentrations nor change the corticosterone levels in rodents. Given that AUD is a major health-care challenge causing an enormous cost to society and novel treatment strategies are warranted, our data suggest that NMU analogues deserve to be evaluated as novel treatment of AUD in humans.
机译：通过调查酒精激活大脑奖励系统的神经化学机制，可以开发新的酒精使用障碍（AUD）的新型治疗策略，慢性复发疾病。与肠脑肽的功能的常见视图相比，例如神经细胞素U（nmu），调节食物摄入和食欲，暗示了加固调解中的新作用。 NMU的厌恶效应通过NMU2受体介导，优选在弧形核和椎间露核中介导。 NMU2受体的表达也在大脑中的几个奖励相关区域中表达，表明奖励规定中的作用。因此，设立了本实验，以研究NMU对啮齿动物醇介导的行为的影响。我们发现NMU的中央施用减毒了醇诱导的运动刺激，组分多巴胺释放和小鼠条件偏好的表达。此外，NMU剂量依赖性降低醇摄入量高，但不含低酒精的大鼠。中部NMU管理没有改变血液醇浓度，也没有改变啮齿动物中的皮质酮水平。鉴于澳大利亚是一个主要的医疗挑战，造成巨大的社会成本，并保证了新的治疗策略，我们的数据表明，NMU类似物值得被评估为对人类的澳元的新待遇。

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