부산대학교 도서관

We have modelled genetic risk for binge‐like drinking by selectively breeding High Drinking in the Dark‐1 and ‐2 (HDID‐1 and HDID‐2) mice for their propensity to reach intoxicating blood alcohol levels (BALs) after binge‐like drinking in a single bottle, limited access paradigm. Interestingly, in standard two‐bottle choice (2BC) tests for continuously available alcohol versus water, HDID mice show modest levels of preference. This indicates some degree of independence of the genetic contributions to risk for binge‐like and sustained, continuous access drinking. We had few data where the drinking in the dark (DID) tests of binge‐like drinking had been repeatedly performed, so we serially offered multiple DID tests to see whether binge‐like drinking escalated. It did not. We also asked whether HDID mice would escalate their voluntary intake with prolonged exposure to alcohol 2BC. They did not. Lastly, we assessed whether an alcohol deprivation effect (ADE) developed. ADE is a temporary elevation in drinking typically observed after a period of abstinence from sustained access to alcohol choice. With repetition, these periods of ADE sometimes have led to more sustained elevations in drinking. We therefore asked whether repeated ADE episodes would elevate choice drinking in HDID mice. They did not. After nearly 500 days of alcohol access, the intake of HDID mice remained stable. We conclude that a genetically‐enhanced high risk for binge‐like drinking is not sufficient to yield alterations in long‐term alcohol intake. [ABSTRACT FROM AUTHOR]