Effects of acute withdrawal on ethanol-induced conditioned place preference in DBA/2J mice

Dreumont, Sarah E.; Cunningham, Christopher L.

doi:10.1007/s00213-013-3291-6

Cited by 5 publications

(4 citation statements)

References 37 publications

(63 reference statements)

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“…Fidler et al (2011) recently proposed several possible mechanisms related to dependence-enhanced intragastric ethanol self-administration in D2 mice: enhanced ethanol positive reward, reduced aversive effects, or relief of negative consequences associated with dependence/withdrawal. Greater reward valuation by D2 mice following dependence would be consistent with both their greater sensitivity in conditioned place-preference paradigms (Cunningham, Niehus, Malott, & Prather, 1992), as well as the finding that pairing acute withdrawal with acute ethanol enhances conditioned place preference for ethanol in this strain (Dreumont & Cunningham, 2014). Because we used a single-bottle self-administration procedure, we could not directly measure ethanol reward as it is represented by preference between ethanol and a non-rewarding solution.…”

Section: Discussionsupporting

confidence: 54%

“…Conversely, D2 mice express pronounced physical and emotional vulnerability to ethanol dependence. This vulnerability is manifested as increased incidence of withdrawal-related seizures (Crabbe, Kosobud, Young, & Janowsky, 1983), enhanced conditioned-taste aversion (Risinger & Cunningham, 1998) and ethanol reward (Dreumont & Cunningham, 2014), and relatively greater c-fos expression (compared to B6) within ‘emotional centers’ such as the lateral/basolateral and central amygdala, bed nucleus of the stria terminalis, hippocampus, and prelimbic cortex (Chen, Reilly, Kozell, Hitzemann, & Buck, 2009). Our finding that D2 mice express enhanced anxiety-like behavior within the light/dark transition assay is entirely consistent with the hypothesis that dependence drives drinking more through mechanisms related to negative affect in this strain.…”

Section: Discussionmentioning

confidence: 99%

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Chronic intermittent ethanol inhalation increases ethanol self-administration in both C57BL/6J and DBA/2J mice

McCool

Chappell

2015

Alcohol

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Inbred mouse strains provide significant opportunities to understand the genetic mechanisms controlling ethanol-directed behaviors and neurobiology. They have been specifically employed to understand cellular mechanisms contributing to ethanol consumption, acute intoxication, and sensitivities to chronic effects. However, limited ethanol consumption by some strains has restricted our understanding of clinically relevant endpoints such as dependence-related ethanol intake. Previous work with a novel tastant-substitution procedure using monosodium glutamate (MSG or umami flavor) has shown that the procedure greatly enhances ethanol consumption by mouse strains that express limited drinking phenotypes using other methods. In the current study, we employ this MSG-substitution procedure to examine how ethanol dependence, induced with passive vapor inhalation, modifies ethanol drinking in C57BL/6J and DBA/2J mice. These strains represent ‘high’ and ‘low’ drinking phenotypes, respectively. We found that the MSG substitution greatly facilitates ethanol drinking in both strains, and likewise, ethanol dependence increased ethanol consumption regardless of strain. However, DBA/2J mice exhibited greater sensitivity dependence-enhanced drinking, as represented by consumption behaviors directed at lower ethanol concentrations and relative to baseline intake levels. DBA/2J mice also exhibited significant withdrawal-associated anxiety-like behavior while C57BL/6J mice did not. These findings suggest that the MSG-substitution procedure can be employed to examine dependence-enhanced ethanol consumption across a range of drinking phenotypes, and that C57BL/6J and DBA/2J mice may represent unique neurobehavioral pathways for developing dependence-enhanced ethanol consumption.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Chronic intermittent ethanol inhalation increases ethanol self-administration in both C57BL/6J and DBA/2J mice

McCool

Chappell

2015

Alcohol

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“…There are no free-choice MA intake studies that have examined the impact of withdrawal period. However, based on alcohol intake studies with DBA/2J (D2) and B6 mice (Cunningham et al, 2013; Dreumont and Cunningham, 2014), we predicted that short acute withdrawal periods within a day between MA access periods would sustain or even enhance MA intake, whereas longer withdrawal periods of days between MA access periods would attenuate MA intake.…”

Section: Introductionmentioning

confidence: 99%

A Mouse Model for Binge-Level Methamphetamine Use

et al. 2016

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Binge/crash cycles of methamphetamine (MA) use are frequently reported by individuals suffering from MA use disorders. A MA binge is self-reported as multiple daily doses that commonly accumulate to 800 mg/day (~10 mg/kg/day for a 170 pound human). A genetic animal model with a similar vulnerability to binge-level MA intake is missing. We used selectively bred MA high drinking (MAHDR) and low drinking (MALDR) mouse lines to determine whether several procedural variations would result in binge-level MA intake. Data were also collected in two progenitor populations of the MA drinking lines, the DBA/2J (D2) strain and the F2 cross of the D2 and C57BL/6J strains. The impact of 3 factors was examined: (1) concentration of MA in the two-bottle choice procedure used for selective breeding; (2) ratio of bottles containing MA vs. water, and (3) length of the withdrawal (or abstinence) period between MA drinking sessions. When MA concentration was progressively increased every 4 days in 20 mg/l amounts from 20 to 140 mg/l, maximum intake in MALDR mice was 1.1 mg/kg, whereas MAHDR mice consumed as much as 14.6 mg/kg. When these concentrations were tested in a multiple bottle choice procedure, the highest ratio of MA to water bottles (3:1) was associated with escalated MA intake of up to 29.1 mg/kg in MAHDR mice and 12.0 mg/kg in F2 mice; MALDR mice did not show a ratio-dependent escalation in MA intake. Finally, MAHDR and D2 mice were offered 3 bottles of MA vs. water at increasing concentrations from 20 to 80 mg/l, and tested under an intermittent 6-h withdrawal period, which was lengthened to 30 h (D2 mice) or to 30 or 78 h (MAHDR). D2 and MAHDR mice initially consumed similar amounts of 14–16 mg/kg MA, but D2 mice reduced their MA intake 3-fold after introduction of 30-h abstinence periods, whereas MAHDR mice retained their high level of intake regardless of withdrawal period. MAHDR mice provide a genetic model of binge-level MA intake appropriate for the study of associated MA-induced neurobiological changes and pharmaceutical treatments.

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“…The acute activation of compensatory brain mechanisms directed towards the preservation of homeostasis can elicit acute (conditioned) withdrawal symptoms once the expected drug of abuse is not consumed (conditioned withdrawal [47,48]). Such conditioned withdrawal reactions [49,50,51,52] suggest that contextual cues elicit counteradaptive mechanisms that are specifically directed against the sedative effects of the drug of abuse. Indeed, cessation of chronic consumption of a GABAergic drug is accompanied by conditioned withdrawal symptoms and a strong urge to consume the drug [17,41].…”

Section: Learning Mechanisms and The Neurobiological Correlates Undermentioning

confidence: 99%

Too Difficult to Stop: Mechanisms Facilitating Relapse in Alcohol Dependence

et al. 2014

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Background: In alcohol and other substance dependencies, patients often suffer relapse despite better knowledge and their intention to remain abstinent. A variety of neurotransmitter systems and their respective alterations due to the chronic drug intake are involved in mechanisms that facilitate relapse. It has been postulated that these neurotransmitter systems are related to changes in motivational and learning mechanisms, and engender a shift from goal-directed to habitual behavior in dependent patients that facilitates drug-seeking behavior. Methods: We review learning mechanisms facilitating relapse, as identified and tested to date. We focus on studies examining the interaction between alcohol-related changes in monoaminergic neurotransmission and their respective effects on pavlovian and operant learning mechanisms in alcohol dependence. Results: Animal experiments and first human studies suggest that chronic alcohol intake impairs goal-directed behavior and facilitates habitual drug intake. Key symptoms of alcohol dependence such as tolerance development, withdrawal, craving and reduced control of alcohol intake can be explained by alcohol-induced alteration of dopaminergic neurotransmission and its GABAergic and glutamatergic modulation and their respective effects on pavlovian and operant conditioning as well as pavlovian-to-instrumental transfer. Conclusion: Chronic alcohol intake impairs neurotransmitter systems that regulate prefrontal-striatal circuits and interfere with goal-directed decision-making and the acquisition of new, non-drug-related behavior patterns. Alcohol craving induced by pavlovian conditioned cues can facilitate habitual drug intake. Such learning mechanisms and their alterations by chronic alcohol intake might be targeted by specific interventions.

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Effects of acute withdrawal on ethanol-induced conditioned place preference in DBA/2J mice

Cited by 5 publications

References 37 publications

Chronic intermittent ethanol inhalation increases ethanol self-administration in both C57BL/6J and DBA/2J mice

Chronic intermittent ethanol inhalation increases ethanol self-administration in both C57BL/6J and DBA/2J mice

A Mouse Model for Binge-Level Methamphetamine Use

Too Difficult to Stop: Mechanisms Facilitating Relapse in Alcohol Dependence

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