Belknap J K, Crabbe J C, Young E R
Research Service (151 W), VA Medical Center, Portland, OR 97201.
Psychopharmacology (Berl). 1993;112(4):503-10. doi: 10.1007/BF02244901.
To determine genetic differences in ethanol consumption, 15 commonly used inbred strains of mice were given ad libitum two-bottle choice between ethanol, 0.2% saccharin, or ethanol plus saccharin in one bottle versus tap water in the other bottle. Three different concentrations of ethanol were used: 3%, 6% and 10% (v/v). Of the 15 strains, the C57BL/6J, C57BR/cdJ and C57L/J strains showed the most consistent higher intake of ethanol either with or without 0.2% saccharin. In marked contrast, the DBA/1J and DBA/2J strains consistently showed the lowest intake. Consumption of 3% ethanol without saccharin was highly genetically correlated with saccharin consumption (r = 0.77), suggesting that low concentrations of ethanol may have a sweet taste that affects voluntary consumption. Most strains showed very different patterns of response to ethanol with or without saccharin. Three patterns of strain responses were identified. Some strains avoided higher concentrations of ethanol whether in water or saccharin; some appeared to be sensitive to the ability of saccharin to mask the odor of ethanol; and some may have reduced consumption only when ethanol concentrations were high enough to produce aversive postingestional effects. Whereas earlier studies generally attempted to explain strain differences in consumption by invoking a single mechanism, our results demonstrate that more than one mechanism is necessary to explain the preferential ethanol intake of all strains studied.
为了确定乙醇摄入量的基因差异,给15种常用的近交系小鼠提供两瓶自由选择的饮品,一瓶是乙醇、0.2%糖精或乙醇加0.2%糖精,另一瓶是自来水。使用了三种不同浓度的乙醇:3%、6%和10%(v/v)。在这15个品系中,C57BL/6J、C57BR/cdJ和C57L/J品系在有或没有0.2%糖精的情况下,乙醇摄入量始终较高。与之形成鲜明对比的是,DBA/1J和DBA/2J品系的摄入量始终最低。饮用不含糖精的3%乙醇与饮用糖精的量高度遗传相关(r = 0.77),这表明低浓度的乙醇可能有甜味,会影响自愿摄入量。大多数品系对含或不含糖精的乙醇表现出非常不同的反应模式。确定了三种品系反应模式。一些品系无论在水中还是在糖精中都避免饮用高浓度的乙醇;一些品系似乎对糖精掩盖乙醇气味的能力敏感;还有一些品系可能只有当乙醇浓度高到足以产生厌恶的摄食后效应时,其摄入量才会减少。早期的研究通常试图通过单一机制来解释品系间摄入量的差异,而我们的结果表明,需要不止一种机制来解释所有研究品系对乙醇的偏好摄入。