Responses to ethanol in C57BL/6 versus C57BL/6 × 129 hybrid mice

Lim, Jana P.; Zou, Mimi E.; Janak, Patricia H.; Messing, Robert O.

doi:10.1002/brb3.29

Cited by 25 publications

(22 citation statements)

References 18 publications

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“…Genetic background also influences the total amount of ethanol consumed in different procedures. Hybrid C57BL/6 X 129S6_SvEvTac mice consume significantly less ethanol compared with C57BL/6 mice in the 24-hour continuous access procedure and the 4-hour limited access procedure (Lim et al, 2012). The level of consumption in our hybrid C57BL/6 X 129S6_SvEvTac wild-type mice was less than that seen with C57BL/6J mice in the 24-hour intermittent ethanol procedure (Hwa et al, 2011; Crabbe et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Deletion ofPrkczIncreases Intermittent Ethanol Consumption in Mice

Lee

Zou

Lim

et al. 2013

Alcohol Clin Exp Res

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Background Prkcz has been identified as a gene whose expression is positively correlated with ethanol consumption in mice and is also induced by ethanol. Two proteins are produced from Prkcz: protein kinase M zeta (PKMζ), which is expressed in the nervous system and protein kinase C zeta (PKCζ), which is expressed in other tissues. We examined Prkcz−/− mice that lack PKCζ and PKMζ to investigate the role of this gene in behavioral responses to ethanol. Methods Male Prkcz−/− and wild-type littermates were tested for ethanol consumption using four procedures: 24-hour intermittent access, 4-hour limited intermittent access, 4-day drinking-in-the-dark (DID), and 24-hour continuous access. We also assessed the acute hypnotic effect of ethanol, ethanol reward, and taste preference for sweet-, bitter-, salty-, and umami-flavored solutions. Finally, we determined whether ethanol could increase PKMζ and PKCζ transcripts and protein expression in wild-type mice using quantitative PCR and western blot analysis. Results Prkcz−/− mice consumed more ethanol than their wild-type littermates in both intermittent access procedures, but not in the DID or 24-hour continuous access procedures. Ethanol exposure increased Prkcz transcripts in cultured PC12 cells and intermittent ethanol consumption increased PKMζ protein in the ventral striatum of wild-type mice. Conclusions Absence of PKMζ in the brain is associated with increased ethanol intake during procedures that incorporate intermittent consumption sessions every other day. Our data suggest that ethanol induces PKMζ, which acts in a negative feedback loop to limit binge-like ethanol consumption.

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Section: Discussionmentioning

confidence: 99%

Deletion ofPrkczIncreases Intermittent Ethanol Consumption in Mice

Lee

Zou

Lim

et al. 2013

Alcohol Clin Exp Res

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“…Ethanol place preference was established by conditioning C57BL/6 mice (male, 18–22g, Taconic) to 2 g/kg (15%) ethanol (Lim et al, 2011). A locomotor box (Med Associates, St Albans, VT) was divided in two chambers.…”

Section: Methodsmentioning

confidence: 99%

Distinctive modulation of ethanol place preference by delta opioid receptor-selective agonists

Rijn

Brissett

Whistler

2012

Drug and Alcohol Dependence

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Background Naltrexone is one of the few drugs approved by the Federal Drug Administration for the treatment of alcoholism. However, naltrexone is only effective in a subpopulation of treatment-seeking alcohol abusers, and suffers from compliance issues. The non-selective nature of this opioid antagonist likely contributes to its side effects and poor therapeutic efficacy. Drugs selectively targeting delta opioid receptor subtypes offer a potential way to treat alcohol abuse disorders. We have recently shown that delta subtype-selective agonists TAN-67 and SNC80 can have opposing effects on alcohol consumption, while having similar effects on alcohol withdrawal-induced anxiety. Methods We studied the ability of TAN-67 and SNC80 to induce place preference in naïve and ethanol exposed C57BL/6 mice and determined the effect of these agonists on the expression of ethanol place preference. Results We show that TAN-67 and SNC80 have opposing actions on ethanol place preference. However, neither of the drugs induces place preference by themselves at doses that are therapeutically effective in mice. Interestingly, SNC80, like naltrexone reduces ethanol place preference, however we have previously shown that SNC80 increases ethanol consumption at the tested dose. Similar to naltrexone, TAN-67 reduces alcohol consumption, but we show here that it may be due to an increase in ethanol place preference. Importantly, we found that chronic ethanol exposure does not increase the rewarding properties of the DOR subtype selective agonists. Conclusions Our results provide a better understanding of how DOR subtype selective drugs could potentially be used for treatment of alcohol abuse disorders.

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“…Two of the most prominent animal models in EtOH research are intermittent access to EtOH (IAE) using 2‐bottle choice (Barak et al., ,b; Carnicella et al., , ; George et al., ; Hopf et al., ; Lee et al., ; Li et al., ; Lim et al., ; Millan et al., ; Momeni et al., ; Seif et al., ; Simms et al., , ; Wise, ) and chronic intermittent EtOH (CIE) vapor exposure (Gilpin et al., ,c; de Guglielmo et al., ; Kissler et al., ; Leao et al., ; Staples et al., ). The IAE paradigm is commonly used to model bingelike drinking and compulsive‐like responding for EtOH (Barak et al., ; Feduccia et al., ; Nielsen et al., ; Simms et al., ) before dependence occurs, whereas CIE has been used to model postdependent states, as well as excessive drinking and compulsive‐like responding for EtOH when combined with EtOH self‐administration (O'Dell et al., ; Roberts et al., , ; Rogers et al., ; Schulteis et al., ).…”

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confidence: 99%

Intermittent Access to Ethanol Drinking Facilitates the Transition to Excessive Drinking After Chronic Intermittent Ethanol Vapor Exposure

Kimbrough

Kim

Cole

et al. 2017

Alcoholism Clin & Exp Res

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Background Alcohol binge drinking in humans is thought to increase the risk for alcohol use disorder. Unclear is whether drinking patterns (e.g., binge-like or stable drinking) differentially affect the transition to compulsive-like drinking in dependent individuals. We examined whether chronic binge-like drinking facilitates the transition to compulsive-like drinking in rats. Methods Male Wistar rats were given 5 months of intermittent access to ethanol (IAE) or continuous access to ethanol (CAE) in a two-bottle choice paradigm. Then rats were given chronic intermittent ethanol (CIE) vapor exposure. Escalation of ethanol intake and compulsive-like responding for ethanol, using a progressive-ratio schedule of reinforcement and quinine-adulterated ethanol, were measured. Results IAE rats escalated ethanol drinking after 2 weeks of two-bottle choice, whereas CAE rats exhibited stable ethanol drinking for 5 months. After 8 weeks of CIE, both IAE+CIE and CAE+CIE rats escalated their ethanol intake. However, IAE rats escalated their ethanol intake weeks sooner than CAE rats and exhibited greater ethanol intake. No differences in compulsive-like responding were found between IAE+CIE and CAE+CIE rats. However, both IAE+CIE and CAE+CIE rats showed strong compulsive-like responding compared with rats without prior IAE or CAE. Conclusions Chronic ethanol drinking at stable or escalated levels for several months is associated with more compulsive-like responding for ethanol in rats that are exposed to CIE compared with rats without a prior history of ethanol drinking. Moreover, IAE facilitated the transition to compulsive-like responding for ethanol after CIE exposure, reflected by the escalation of ethanol intake. These results suggest that IAE may facilitate the transition to alcohol use disorder. The present study indicates that despite a moderate level of ethanol drinking, the IAE animal model is highly relevant to early stages of alcohol abuse and suggests that it may be associated with neuroadaptations that produce a faster transition to alcohol dependence.

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Responses to ethanol in C57BL/6 versus C57BL/6 × 129 hybrid mice

Cited by 25 publications

References 18 publications

Deletion ofPrkczIncreases Intermittent Ethanol Consumption in Mice

Deletion ofPrkczIncreases Intermittent Ethanol Consumption in Mice

Distinctive modulation of ethanol place preference by delta opioid receptor-selective agonists

Intermittent Access to Ethanol Drinking Facilitates the Transition to Excessive Drinking After Chronic Intermittent Ethanol Vapor Exposure

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