Schedule of Passive Ethanol Exposure Affects Subsequent Intragastric Ethanol Self‐Infusion

Fidler, Tara L.; Oberlin, Brandon G.; Struthers, Amanda M.; Cunningham, Christopher L.

doi:10.1111/j.1530-0277.2009.01029.x

Cited by 8 publications

(18 citation statements)

References 37 publications

(71 reference statements)

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“…Previous studies have shown that rats will sign-track an ethanol-associated cue, and that the effect of ethanol on tests of impulsivity are associated with sign-tracking behavior (Tomie et al 1998a; 1998b; Krank et al 2008; Krank 2003). However, ethanol has potent aversive effects when administered acutely, and requires previous exposure to overcome this initial aversion (Schramm-Sapyta et al 2010; Fidler et al 2009; Bormann and Cunningham 1998; Asin et al 1985; van der Kooy et al 1983; Cunningham et al 2002). Thus, we predicted that ethanol would decrease the incentive value of a food-associated cue.…”

Section: Introductionmentioning

confidence: 99%

The tendency to sign-track predicts cue-induced reinstatement during nicotine self-administration, and is enhanced by nicotine but not ethanol

2016

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Rationale Some individuals are particularly responsive to reward-associated stimuli (“cues”), including the effects of these cues on craving and relapse to drug-seeking behavior. In the cases of nicotine and alcohol, cues may acquire these abilities via the incentive-enhancing properties of the drug. Objectives To determine the interaction between cue-responsivity and nicotine reinforcement, we studied the patterns of nicotine self-administration in rats categorized based on their tendency to approach a food predictive cue (“sign-trackers”) or a reward-delivery location (“goal-trackers”). In a second experiment, we determined whether nicotine and ethanol altered the incentive value of a food cue. Methods Rats were classified as sign- or goal-trackers during a Pavlovian conditioned approach paradigm. Rats then self-administered intravenous nicotine (0.03 mg/kg infusions) followed by extinction and cue induced reinstatement tests. We also tested the effects of nicotine (0.4 mg/kg base s.c.) or ethanol (0.7 g/kg i.p.) on the approach to, and reinforcing efficacy of, a food cue. Results Sign-trackers showed greater reinstatement in response to a nicotine cue. Further, nicotine enhanced sign-tracking but not goal-tracking to a food cue, and also enhanced responding for the food cue during the conditioned reinforcement test. Conversely, ethanol reduced sign-tracking and increased goal-tracking, but had no effect on conditioned reinforcement. Conclusions Our studies demonstrate that the tendency to attribute incentive value to a food cue predicts enhanced cue-induced reinstatement. Additionally, the incentive value of food cues is differentially modulated by nicotine and ethanol, which may be related to the reinforcing effects of these drugs.

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Section: Introductionmentioning

confidence: 99%

The tendency to sign-track predicts cue-induced reinstatement during nicotine self-administration, and is enhanced by nicotine but not ethanol

2016

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“…Fidler and Cunningham have revived a technique developed by Deutsch in the 1970s using intragastric catheters for ethanol delivery, which bypasses orosensory cues that might impede high levels of ethanol intake. These investigators have shown that passive infusions of ethanol by an intragastric catheter are capable of rendering rodents ethanol-dependent and subsequently increasing self-infusions of ethanol compared to those not experiencing passive infusions of ethanol (Fidler et al, 2006; Fidler et al, 2011; Fidler, Oberlin, Struthers, & Cunningham, 2009; Fidler et al, 2012). However, in recent years, the procedure most often used to render mice and rats dependent on ethanol and to increase free-choice drinking or operant self-administration is the use of vapor inhalation procedures akin to those developed in the early 1970s (Goldstein & Pal, 1971).…”

Section: Introductionmentioning

confidence: 99%

Alcohol dependence and free-choice drinking in mice

Griffin

2014

Alcohol

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Alcohol dependence continues to be an important health concern and animal models are critical to furthering our understanding of this complex disease. A hallmark feature of alcoholism is a significant increase in alcohol drinking over time. While several different animal models of excessive alcohol (ethanol) drinking exist for mice and rats, a growing number of laboratories are using a model that combines chronic ethanol exposure procedures with voluntary ethanol drinking with mice as experimental subjects. Primarily, these studies use a chronic intermittent ethanol (CIE) exposure pattern to render mice dependent and a 2-h limited access procedure to evaluate drinking behavior. Compared to non-dependent mice that also drink ethanol, the ethanol-dependent mice demonstrate significant increases in voluntary ethanol drinking. The increased drinking significantly elevates blood and brain ethanol concentrations compared to the non-dependent control mice. Studies report that the increased drinking by dependent mice is driven by neuroadaptations in glutamatergic and corticotropin-releasing factor signaling in different brain regions known to be involved in alcohol-related behaviors. The dysregulation of these systems parallels findings in human alcoholics and treatments that demonstrate efficacy in alcoholics can also reduce drinking in this model. Moreover, preclinical findings have informed the development of human clinical trials, further highlighting the translational potential of the model. As a result of these features, the CIE exposure and free-choice drinking model is becoming more widely used and promises to provide more insight into mechanisms of excessive drinking that may be important for developing treatments for human alcoholics. The salient features and possible future considerations for CIE exposure and free-choice drinking in mice are discussed.

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“…Although the literature offers several examples of enhanced ethanol intake during the first day of withdrawal in rats [7-11], strong evidence that this effect is reduced when access is delayed for several days (after acute withdrawal subsides) is lacking. The only experiments that have directly compared groups of rats initially given ethanol at different times during withdrawal found no differences in ethanol intake [10, 12], but all of these groups were probably in acute withdrawal at the time of initial access (≤ 36 h after withdrawal). On the basis of cross-experiment comparisons, other reports have suggested that rats self-administer less when initial ethanol access is delayed for 2 weeks after withdrawal compared to access within the first 12 h [9, 11], but no single experiment has directly compared ethanol intakes between post-dependent rats given initial ethanol access during acute withdrawal and post-dependent rats given initial ethanol access after acute withdrawal has dissipated.…”

Section: Introductionmentioning

confidence: 99%

Time-Dependent Negative Reinforcement of Ethanol Intake by Alleviation of Acute Withdrawal

Cunningham

Fidler

Murphy

et al. 2013

Biological Psychiatry

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Background Drinking to alleviate the symptoms of acute withdrawal is included in diagnostic criteria for alcoholism, but the contribution of acute withdrawal relief to high alcohol intake has been difficult to model in animals. Methods Ethanol dependence was induced by passive intragastric ethanol infusions in C57BL/6J (B6) and DBA/2J (D2) mice; non-dependent controls received water infusions. Mice were then allowed to self-administer ethanol or water intragastrically. Results The time course of acute withdrawal was similar to that produced by chronic ethanol vapor exposure in mice, reaching a peak at 7-9 h and returning to baseline within 24 h; withdrawal severity was greater in D2 than in B6 mice (Exp. 1). Post-withdrawal delays in initial ethanol access (1, 3 or 5 days) reduced the enhancement in later ethanol intake normally seen in D2 (but not B6) mice allowed to self-infuse ethanol during acute withdrawal (Exp. 2). The post-withdrawal enhancement of ethanol intake persisted over a 5-d abstinence period in D2 mice (Exp. 3). D2 mice allowed to drink ethanol during acute withdrawal drank more ethanol and self-infused more ethanol than non-dependent mice (Exp. 4). Conclusions Alcohol access during acute withdrawal increased later alcohol intake in a time-dependent manner, an effect that may be related to a genetic difference in sensitivity to acute withdrawal. This promising model of negative reinforcement encourages additional research on the mechanisms underlying acute withdrawal relief and its role in determining risk for alcoholism.

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Schedule of Passive Ethanol Exposure Affects Subsequent Intragastric Ethanol Self‐Infusion

Cited by 8 publications

References 37 publications

The tendency to sign-track predicts cue-induced reinstatement during nicotine self-administration, and is enhanced by nicotine but not ethanol

The tendency to sign-track predicts cue-induced reinstatement during nicotine self-administration, and is enhanced by nicotine but not ethanol

Alcohol dependence and free-choice drinking in mice

Time-Dependent Negative Reinforcement of Ethanol Intake by Alleviation of Acute Withdrawal

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