Using drinking in the dark to model prenatal binge‐like exposure to ethanol in C57BL/6J mice

Boehm, Stephen L.; Moore, Eileen M.; Walsh, Cherie D; Gross, Carly D.; Cavelli, Austin M; Gigante, Eduardo D.; Linsenbardt, David N.

doi:10.1002/dev.20320

Cited by 47 publications

(47 citation statements)

References 43 publications

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“…The limited access “drinking in the dark” alcohol exposure paradigm used in the present study is a voluntary consumption paradigm modified from a mouse model originally established by Boehm and colleagues [34]. The limited access to 10% ethanol for 4 hours daily results in average BECs in mouse dams of 88 mg/dl throughout the gestational period [16].…”

Section: Discussionmentioning

confidence: 99%

Fate Analysis of Adult Hippocampal Progenitors in a Murine Model of Fetal Alcohol Spectrum Disorder (FASD)

2013

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Prenatal alcohol exposure can lead to fetal alcohol spectrum disorder (FASD) and associated behavioral impairments that may be linked to disruptions in adult hippocampal neurogenesis. Social and physical enrichment has been proposed as a potential therapeutic approach toward reversing behavioral deficits associated with FASD and is also a potent stimulator of adult hippocampal neurogenesis. In the present study, we utilized a genetic fate mapping approach in nestin-CreERT2/YFP bitransgenic mice to identify the stage-specific impact of prenatal alcohol exposure on the stepwise maturation of adult hippocampal progenitors. Using a limited alcohol access “drinking-in-the-dark” model of FASD, we confirm previous findings that moderate prenatal alcohol exposure has no effect on adult neurogenesis under standard housing conditions, but abolishes the neurogenic response to enriched environment (EE). Furthermore, we demonstrate that this effect is primarily due to failed EE-mediated survival of postmitotic neurons. Finally, we demonstrate that the neurogenic deficit is associated with impaired spatial pattern recognition, as demonstrated by delayed learning of FASD-EE mice in an A–B contextual discrimination task. These results identify a potential maturational stage-specific mechanism(s) underlying impaired neurogenic function in a preclinical model of FASD, and provide a basis for testing regulatory pathways in this model through conditional and inducible manipulation of gene expression in the adult hippocampal progenitor population.

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Section: Discussionmentioning

confidence: 99%

Fate Analysis of Adult Hippocampal Progenitors in a Murine Model of Fetal Alcohol Spectrum Disorder (FASD)

2013

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“…This procedure parallels the DID procedure used in mice (e.g., Boehm et al, 2008; Crabbe et al, 2009; Lyons et al, 2008; Moore and Boehm, 2009; Navarro et al, 2009; Rhodes et al, 2005). However, initial access to ethanol during the dark-cycle must occur immediately upon lights out to maximize intake in rats, whereas initial access for mice must occur after three or fours into the dark cycle (Bell et al, 2006c; Rhodes et al, 2005; but see Colombo et al, 2014).…”

Section: Background From An Animal Model Perspectivementioning

confidence: 99%

Rat animal models for screening medications to treat alcohol use disorders

et al. 2017

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The purpose of this review is to present animal research models that can be used to screen and/or repurpose medications for the treatment of alcohol abuse and dependence. The focus will be on rats and in particular selectively bred rats. Brief introductions discuss various aspects of the clinical picture, which provide characteristics of individuals with alcohol use disorders (AUDs) to model in animals. Following this, multiple selectively bred rat lines will be described and evaluated in the context of animal models used to screen medications to treat AUDs. Next, common behavioral tests for drug efficacy will be discussed particularly as they relate to stages in the addiction cycle. Tables highlighting studies that have tested the effects of compounds using the respective techniques are included. Wherever possible the Tables are organized chronologically in ascending order to describe changes in the focus of research on AUDs over time. In general, high ethanol-consuming selectively bred rats have been used to test a wide range of compounds. Older studies usually followed neurobiological findings in the selected lines that supported an association with a propensity for high ethanol intake. Most of these tests evaluated the compound's effects on the maintenance of ethanol drinking. Very few compounds have been tested during ethanol-seeking and/or relapse and fewer still have assessed their effects during the acquisition of AUDs. Overall, while a substantial number of neurotransmitter and neuromodulatory system targets have been assessed; the roles of sex- and age-of-animal, as well as the acquisition of AUDs, ethanol-seeking and relapse continue to be factors and behaviors needing further study.

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“…These studies suggest that the DID phenotype is not primarily related to feeding behavior, or at least to calorie-seeking (Lyons et al 2008). In another application of the method, Boehm et al have used the DID procedure to offer high ethanol concentrations to pregnant C57BL/6J mice in an attempt to model binge-like consumption (Boehm et al 2008). These animals reached BECs of 118–182 mg%, sufficient to produce behavioral changes in adolescent offspring.…”

Section: Beyond Alcohol Preference Drinkingmentioning

confidence: 99%

The Complexity of Alcohol Drinking: Studies in Rodent Genetic Models

2010

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Risk for alcohol dependence in humans has substantial genetic contributions. Successful rodent models generally attempt to address only selected features of the human diagnosis. Most such models target the phenotype of oral administration of alcohol solutions, usually consumption of or preference for an alcohol solution versus water. Data from rats and mice for more than 50 years have shown genetic influences on preference drinking and related phenotypes. This paper summarizes some key findings from that extensive literature. Much has been learned, including the genomic location and possible identity of several genes influencing preference drinking. We report new information from congenic lines confirming QTLs for drinking on mouse chromosomes 2 and 9. There are many strengths of the various phenotypic assays used to study drinking, but there are also some weaknesses. One major weakness, the lack of drinking excessively enough to become intoxicated, has recently been addressed with a new genetic animal model, mouse lines selectively bred for their high and intoxicating blood alcohol levels after a limited period of drinking in the circadian dark. We report here results from a second replicate of that selection and compare them with the first replicate.

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Using drinking in the dark to model prenatal binge‐like exposure to ethanol in C57BL/6J mice

Cited by 47 publications

References 43 publications

Fate Analysis of Adult Hippocampal Progenitors in a Murine Model of Fetal Alcohol Spectrum Disorder (FASD)

Fate Analysis of Adult Hippocampal Progenitors in a Murine Model of Fetal Alcohol Spectrum Disorder (FASD)

Rat animal models for screening medications to treat alcohol use disorders

The Complexity of Alcohol Drinking: Studies in Rodent Genetic Models

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