Browsing by Subject "selectively bred"

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    Innate and Acquired Quinine‐Resistant Alcohol, but not Saccharin, Drinking in Crossed High–Alcohol‐Preferring Mice
    (Wiley, 2019-11) Houck, Christa A.; Carron, Claire R.; Millie, Lauren A.; Grahame, Nicholas J.; Psychology, School of Science
    Background Alcohol consumption despite aversive consequences is often a key component of an alcoholism diagnosis. Free‐choice alcohol consumption despite bitter quinine adulteration in rodents has been seen following several months of free‐choice drinking, but there has been little study of whether prolonged access to other palatable substances such as saccharin yields quinine resistance. Selectively bred crossed high–alcohol‐preferring (cHAP) mice average blood alcohol levels of over 250 mg/dl during free‐choice access, considerably higher than other models. We hypothesized that higher intakes would yield more rapid development of quinine‐resistant alcohol (QRA) drinking and quinine‐resistant saccharin (QRS) drinking. Methods All experiments used male and female cHAP mice. Experiment 1 compared mice with either 0 or 5 weeks of alcohol drinking history, testing varying (0.032, 0.10, 0.32 g/l) quinine concentrations in ethanol. Experiment 2 examined whether innate QR may exist, comparing animals with a 1 or zero day of drinking history. Experiment 3 examined the effect of varying histories (0, 2, or 5 weeks) of free‐choice 10% alcohol drinking on QR alcohol consumption at high quinine concentrations. Finally, Experiment 4 investigated the development of QRS drinking. Results We found that we could not detect a history effect in commonly used quinine concentrations, indicating that cHAP mice are innately quinine resistant to 0.10 g/l quinine. However, we were able to determine that a 2‐week drinking history was sufficient to induce QRA drinking in cHAP mice at extremely high quinine concentrations (0.74 and 0.32 g/l). However, the history effect was specific to QRA, a saccharin drinking history, did not yield QRS drinking. Conclusions These data suggest that an alcohol drinking history induces maladaptive behaviors, such as drinking in spite of negative consequences, a pattern not seen with saccharin. Furthermore, a strong genetic predisposition to drink may promote an innate aversion resistance compared with commonly used inbred strains.
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    Pharmacological Modulation of Habit Expression
    (2016-08-17) Houck, Christa A.; Grahame, Nicholas J.; Czachowski, Cristine Lynn; Goodlett, Charles R.
    Habit expression is emerging as a theory of addiction: subjects begin to use drugs to attain positive reinforcing effects but continue to use in spite of negative effects because the behavior becomes habitual, and therefore divorced from its outcome. Many studies have shown that a history of drug and alcohol use lead to expedited acquisition of a habit, but the acute effects of these drugs on behavior is still unknown. Behaviors that result from acute intoxication, such as increased aggression, risky sexual behavior, and impaired judgment, could be interpreted as habitual: actions performed without regard for the outcome. Therefore, we studied the transition from goal-directed to habitual behavior, when a response is made regardless of outcome value, and how acute intoxication of ethanol (EtOH), amphetamine (AMP), nicotine (NIC), and yohimbine (YOH) affect the resulting behavior. Through a series of four experiments, selectively bred crossed High Alcohol Preferring (cHAP) mice were trained on an operant task to self-administer 1% banana solution, which was subsequently devalued via LiCl CTA. EtOH (1 & 1.5 g/kg), AMP (2.0 mg/kg), NIC (0.5 mg/kg), YOH (1.0 mg/kg), or SAL were administered prior to baseline and post-devaluation tests. We found that acute EtOH at 1- and 1.5-g/kg doses facilitated the expression of a habit, whereas all other pretreatments resulted in devaluation. These data may indicate a unique role for EtOH in facilitating the retrieval of habitual over outcome-based associations. This could shed light on why intoxicated individuals display impaired judgment and a mechanism by which relapse after a period of abstinence can occur.