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Browsing by Author "Crabbe, John C."
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Item "Drinking in the Dark" (DID): a simple mouse model of binge-like alcohol intake(Wiley, 2014-07) Thiele, Todd E.; Crabbe, John C.; Boehm, Stephen L. II; Psychology, School of ScienceOne of the greatest challenges that scientists face when studying the neurobiology and/or genetics of alcohol (ethanol) consumption is that most preclinical animal models do not voluntarily consume enough ethanol to achieve pharmacologically meaningful blood ethanol concentrations (BECs). Recent rodent models have been developed that promote binge-like levels of ethanol consumption associated with high BECs (i.e., ≥100 mg/dl). This unit describes procedures for an animal model of binge-like ethanol drinking which has come to be called "drinking in the dark" (DID). The "basic" variation of DID involves replacing the water bottle with a bottle containing 20% ethanol for 2 to 4 hr, beginning 3 hr into the dark cycle, on cages of singly-housed C57BL/6J mice. Using this procedure, mice typically consume enough ethanol to achieve BECs >100 mg/dl and to exhibit behavioral evidence of intoxication. An alternative two-bottle (ethanol and water) procedure is also described.Item Genetic relationship between predisposition for binge alcohol consumption and blunted sensitivity to adverse effects of alcohol in mice(Wiley Blackwell (Blackwell Publishing), 2014-05) Fritz, Brandon M.; Cordero, Kristy A.; Barkley-Levenson, Amanda M.; Metten, Pamela; Crabbe, John C.; Boehm, Stephen L.; Department of Psychology, IU School of ScienceBACKGROUND: Initial sensitivity to ethanol (EtOH) and the capacity to develop acute functional tolerance (AFT) to its adverse effects may influence the amount of alcohol consumed and may also predict future alcohol use patterns. The current study assessed sensitivity and AFT to the ataxic and hypnotic effects of EtOH in the first replicate of mice (HDID-1) selectively bred for high blood EtOH concentrations (BECs) following limited access to EtOH in the Drinking in the Dark (DID) paradigm. METHODS: Naïve male and female HDID-1 and HS/Npt mice from the progenitor stock were evaluated in 3 separate experiments. In Experiments 1 and 2, EtOH-induced ataxia was assessed using the static dowel task. In Experiment 3, EtOH-induced hypnosis was assessed by using modified restraint tubes to measure the loss of righting reflex (LORR). RESULTS: HDID-1 mice exhibited reduced initial sensitivity to both EtOH-induced ataxia (p < 0.001) and hypnosis (p < 0.05) relative to HS/Npt mice. AFT was calculated by subtracting the BEC at loss of function from the BEC at recovery (Experiments 1 and 3) or by subtracting BEC at an initial recovery from the BEC at a second recovery following an additional alcohol dose (Experiment 2). The dowel test yielded no line differences in AFT, but HS/Npt mice developed slightly greater AFT to EtOH-induced LORR than HDID-1 (p < 0.05). CONCLUSIONS: These results suggest that HDID-1 mice exhibit aspects of blunted ataxic and hypnotic sensitivity to EtOH which may influence their high EtOH intake via DID, but do not display widely different development of AFT. These findings differ from previous findings with the high alcohol-preferring (HAP) selected mouse lines, suggesting that genetic predisposition for binge, versus other forms of excessive alcohol consumption, is associated with unique responses to EtOH-induced motor incoordination.