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Persistent Enhancement of Ethanol Drinking Following a Monosodium Glutamate-Substitution Procedure in C57BL6/J and DBA/2J Mice

机译:味精替代C57BL6 / J和DBA / 2J小鼠后持续不断地提高乙醇的饮酒量

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摘要

Inbred mouse strains such as C57BL/6J (B6) and DBA/2J (D2) and related strains have been used extensively to help identify genetic controls for a number of ethanol-related behaviors, including acute intoxication and sensitivity to repeated exposures. The disparate ethanol drinking behaviors of B6 mice expressing high-drinking/preference and D2 mice expressing low-drinking/preference have yielded considerable insight into the heritable control of alcohol drinking. However, the B6-high and D2-low drinking phenotypes are contrasted with ethanol-conditioned reward-like behaviors, which are robustly expressed by D2 mice and considerably less expressed by B6 mice. This suggests that peripheral factors, chiefly ethanol taste, may help drive ethanol drinking by these and related strains, which complicates mouse genetic studies designed to understand the relationships between reward-related behaviors and ethanol drinking. Traditional approaches such as the sucrose/saccharin-substitution procedure that normally accentuate ethanol drinking in rodents have had limited success in low drinking/preferring mice such as the D2 line. This may be due to allelic variations of the sweet taste receptor subunit, expressed by many ethanol low-drinking/preferring strains, which would limit the utility of these types of substitution approaches. We have recently shown () that monosodium glutamate (MSG), the primary component of umami taste, can be used in a substitution procedure to initiate ethanol drinking in both B6 and D2 mice that greatly surpasses that initiated by a more traditional sucrose-substitution procedure. In this study, we show that ethanol drinking initiated by MSG substitution in D2 mice, but not sucrose substitution, can persist for several weeks following removal of the flavor. These findings further illustrate the utility of MSG substitution to initiate ethanol drinking in distinct mouse strains.
机译:自交系小鼠品系,例如C57BL / 6J(B6)和DBA / 2J(D2)及其相关品系已被广泛用于帮助鉴定许多乙醇相关行为的遗传控制,包括急性中毒和对反复暴露的敏感性。表达高饮/偏好的B6小鼠和表达低饮/偏好的D2小鼠的不同乙醇饮酒行为已经对酒精饮酒的遗传控制产生了可观的了解。但是,高B6和低D2的饮酒表型与乙醇调节的奖励样行为相反,后者由D2小鼠强烈表达而在B6小鼠中表达较少。这表明外围因素,主要是乙醇的味道,可能有助于促使这些和相关菌株饮酒,这使旨在了解奖励相关行为与饮酒之间关系的小鼠基因研究变得复杂。传统的方法(如蔗糖/糖精替代程序)通常会增加啮齿动物的乙醇饮用量,但在诸如D2品系的低饮用量/偏爱小鼠中,成功的方法有限。这可能是由于甜味受体亚基的等位基因变异(由许多低酒精度/优选乙醇的菌株表达)所致,这将限制这些类型的替代方法的实用性。我们最近发现(),鲜味的主要成分谷氨酸钠(MSG)可用于替代程序,以在B6和D2小鼠中启动乙醇饮用,大大超过了更传统的蔗糖替代程序所启动的乙醇饮用。在这项研究中,我们显示D2小鼠中由MSG替代引发的乙醇饮用,而不是蔗糖替代,可以在去除风味后持续数周。这些发现进一步说明了MSG取代在不同小鼠品系中启动乙醇饮用的实用性。

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