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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Naltrexone and alcohol drinking in mice lacking beta-endorphin by site-directed mutagenesis.
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Naltrexone and alcohol drinking in mice lacking beta-endorphin by site-directed mutagenesis.

机译：通过定点诱变在缺乏β-内啡肽的小鼠中饮用纳曲酮和酒精。

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Alcohol-induced activation of the opioid system may contribute to the reinforcing properties of alcohol. This study investigated whether elimination of beta-endorphin (BE) synthesis via site-directed mutagenesis in embryonic stem cells would alter alcohol intake in mice. Both BE-deficient and wildtype (WT) mice generated from the targeted stem cells were backcrossed for nine generations onto a C57BL/6 background, and were maintained with ad libitum food and water. Mice had access to alcohol (10% v/v) under the following conditions: 24 h, scheduled access for 2 h/day, following acute (1 or 2 days) or chronic (5 weeks) alcohol deprivation, and scheduled access following six doses of naltrexone (0.125-16.0 mg/kg BW, ip) or saline treatment. Alcohol intake was similar in BE-deficient and WT mice given chronic access to alcohol, but greater in BE-deficient compared with WT mice during the first 10 days of scheduled access to alcohol, but not after more extensive experience with scheduled access. BE-deficient, but not WT mice, increased alcohol intake following 2 days, but not 1 day or 5 weeks, of deprivation. Naltrexone reduced alcohol drinking both in BE-deficient and WT mice, suggesting that drinking is mediated, in part, by activation of opioid receptors in both genotypes.
机译：酒精诱导的阿片样物质系统的活化可能有助于增强酒精的性能。这项研究调查了通过胚胎干细胞中的定点诱变消除β-内啡肽（BE）合成是否会改变小鼠的酒精摄入。从目标干细胞产生的BE缺陷型和野生型（WT）小鼠回交九代至C57BL / 6背景，并随意补充食物和水。在以下情况下，小鼠可以饮酒（10％v / v）：24小时，每天2小时，排定的（1或2天）或慢性（5周）酒精缺乏后，每天6小时以下剂量的纳曲酮（0.125-16.0 mg / kg BW，ip）或生理盐水治疗。长期摄入酒精的BE缺乏和WT小鼠的酒精摄入量相似，但在预定酒精摄入的前10天内，与WT小鼠相比，BE缺乏小鼠的酒精摄入量更高，但在经过定期摄入酒精的丰富经验后却没有。缺乏BE的老鼠（而非WT老鼠）在剥夺2天后（而非1天或5周）会增加酒精摄入。纳曲酮可减少BE缺乏和WT小鼠的饮酒，提示饮酒部分是由两种基因型的阿片受体激活引起的。

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