Similar Ethanol Drinking in Adolescent and Adult <scp>C</scp>57<scp>BL</scp>/6<scp>J</scp> Mice After Chronic Ethanol Exposure and Withdrawal

Carrara-Nascimento, Priscila Fernandes; López, Marcelo F.; Becker, Howard C.; Camarini, Rosana

doi:10.1111/acer.12056

Cited by 17 publications

(22 citation statements)

References 52 publications

(78 reference statements)

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“…This withdrawal model used in this experiment has been successfully used in previous studies investigating the induction of physical dependence and withdrawal signs through abrupt cessation of binge ethanol intake (9–15 g/kg/day) for 3–4 days (Majchrowicz, 1975, Abulseoud et al, 2014). Withdrawal-induced escalation of ethanol drinking, observed in this study, is consistent with previous studies showing elevated ethanol drinking following intermittent ethanol exposure and/or withdrawal period (Carrara-Nascimento et al, 2013, Abulseoud et al, 2014). …”

Section: Discussionsupporting

confidence: 93%

Binge ethanol withdrawal: Effects on post-withdrawal ethanol intake, glutamate–glutamine cycle and monoamine tissue content in P rat model

Das

Althobaiti

Alshehri

et al. 2016

Behavioural Brain Research

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Alcohol withdrawal syndrome (AWS) is a medical emergency situation which appears after abrupt cessation of ethanol intake. Decreased GABA-A function and increased glutamate function are known to exist in the AWS. However, the involvement of glutamate transporters in the context of AWS requires further investigation. In this study, we used a model of ethanol withdrawal involving abrupt cessation of binge ethanol administration (4 g/kg/gavage three times a day for three days) using male alcohol-preferring (P) rats. After 48 hours of withdrawal, P rats were re-exposed to voluntary ethanol intake. The amount of ethanol consumed was measured during post-withdrawal phase. In addition, the expression of GLT-1, GLAST and xCT were determined in both medial prefrontal cortex (mPFC) and nucleus accumbens (NAc). We also measured glutamine synthetase (GS) activity, and the tissue content of glutamate, glutamine, dopamine and serotonin in both mPFC and NAc. We found that binge ethanol withdrawal escalated post-withdrawal ethanol intake, which was associated with downregulation of GLT-1 expression in both mPFC and NAc. The expression of GLAST and xCT were unchanged in the ethanol-withdrawal (EW) group compared to control group. Tissue content of glutamate was significantly lower in both mPFC and NAc, whereas tissue content of glutamine was higher in mPFC but unchanged in NAc in the EW group compared to control group. The GS activity was unchanged in both mPFC and NAc. The tissue content of DA was significantly lower in both mPFC and NAc, whereas tissue content of serotonin was unchanged in both mPFC and NAc. These findings provide important information of the critical role of GLT-1 in context of AWS.

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Section: Discussionsupporting

confidence: 93%

Binge ethanol withdrawal: Effects on post-withdrawal ethanol intake, glutamate–glutamine cycle and monoamine tissue content in P rat model

Das

Althobaiti

Alshehri

et al. 2016

Behavioural Brain Research

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“…Previous work has described an array of neural and behavioral effects of CIE in male mice of several strains (though predominantly C57BL/6J) and various lines of male or sex-balanced groups of gene mutant mice (Becker, 2013). The reported behavioral effects of CIE in mice include elevated ethanol drinking (Becker & Lopez, 2004; Carrara-Nascimento, Lopez, Becker, Olive, & Camarini, 2013; Dhaher, Finn, Snelling, & Hitzemann, 2007; Finn et al, 2007; Griffin, Lopez, & Becker, 2009; Griffin, Lopez, Yanke, Middaugh, & Becker, 2009; Holmes et al, 2012; Lopez & Becker, 2005; McCool & Chappell, 2015), increased seizure susceptibility and anxiety-like behavior (Becker, 1994; Becker, Diaz-Granados, & Hale, 1997; Becker, Diaz-Granados, & Weathersby, 1997; Becker & Hale, 1993; Morales et al, 2015), tolerance to acute ethanol intoxication (Daut et al, 2015), and alterations in appetitive and aversive learning (DePoy et al, 2013, 2015; Holmes et al, 2012; Radke et al, 2015). In terms of sex differences, one study reported that male but not female HAP-2 mice showed increased ethanol drinking and withdrawal signs following CIE (Lopez et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Sex differences in the behavioral sequelae of chronic ethanol exposure

Jury

DiBerto

Kash

et al. 2017

Alcohol

107

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Rates of alcohol use disorders (AUDs) differ between men and women, and there is also marked variation between sexes in the effects of acute and chronic alcohol. In parallel to observations in humans, prior studies in rodents have described male/female differences across a range of ethanol-related behaviors, including ethanol drinking. Nonetheless, there remain gaps in our knowledge of the role of sex in moderating the effects of ethanol, particularly in models of chronic ethanol exposure. The goal of the current study was to assess various behavioral sequelae of exposing female C57BL/6J mice to chronic intermittent ethanol (CIE) via ethanol vapors. Following four weeks of CIE exposure, adult male and female mice were compared for ethanol drinking in a two-bottle paradigm, for sensitivity to acute ethanol intoxication (via loss of righting reflex [LORR]) and for anxiety-like behaviors in the novelty-suppressed feeding and marble burying assays. Next, adult and adolescent females were tested on two different two-bottle drinking preparations (fixed or escalating ethanol concentration) after CIE. Results showed that males and females exhibited significantly blunted ethanol-induced LORR following CIE, whereas only males showed increased anxiety-like behavior after CIE. Increased ethanol drinking after CIE was also specific to males, but high baseline drinking in females may have occluded detection of a CIE-induced effect. The failure to observe elevated drinking in females in response to CIE was also seen in females exposed to CIE during adolescence, regardless of whether a fixed or escalating ethanol-concentration two-bottle procedure was employed. Collectively, these data add to the literature on sex differences in ethanol-related behaviors and provide a foundation for future studies examining how the neural consequences of CIE might differ between males and females.

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“…Chronic intermittent ethanol vapor exposure (CIE) is a well-characterized mouse model of alcohol exposure that elicits an abstinence-induced escalation in voluntary ethanol consumption similar to that observed in human alcoholics (Becker, 2013; Becker and Lopez, 2004; Becker and Ron, 2014; Carrara-Nascimento et al, 2013; Crabbe et al, 2014; DePoy et al, 2013; Griffin, 2014; Griffin et al, 2009; Kissler et al, 2014; Lopez and Becker, 2005; Lopez et al, 2014; Repunte-Canonigo et al, 2014), as well as deficiencies in several other learned and affective behaviors, including attention set-shifting (Kroener et al, 2012), fear extinction (Holmes et al, 2012), reversal learning (Badanich et al, 2011), and anxiety and negative affect (Lowery-Gionta et al, 2014). These behaviors have been shown to be dependent on the PFC, CeA, and BNST, and withdrawal from CIE in mice produces alterations in several aspects of neural function in these regions.…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic ethanol exposure on neuronal function in the prefrontal cortex and extended amygdala

et al. 2015

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Chronic alcohol consumption and withdrawal leads to anxiety, escalated alcohol drinking behavior, and alcohol dependence. Alterations in the function of key structures within the cortico-limbic neural circuit have been implicated in underlying the negative behavioral consequences of chronic alcohol exposure in both humans and rodents. Here, we used chronic intermittent ethanol vapor exposure (CIE) in male C57BL/6J mice to evaluate the effects of chronic alcohol exposure and withdrawal on anxiety-like behavior and basal synaptic function and neuronal excitability in prefrontal cortical and extended amygdala brain regions. Forty-eight hours after four cycles of CIE, mice were either assayed in the marble burying test (MBT) or their brains were harvested and whole-cell electrophysiological recordings were performed in the prelimbic and infralimbic medial prefrontal cortex (PLC and ILC), the lateral and medial central nucleus of the amygdala (lCeA and mCeA), and the dorsal and ventral bed nucleus of the stria terminalis (dBNST and vBNST). Ethanol-exposed mice displayed increased anxiety in the MBT compared to air-exposed controls, and alterations in neuronal function were observed in all brain structures examined, including several distinct differences between subregions within each structure. Chronic ethanol exposure induced hyperexcitability of the ILC, as well as a shift toward excitation in synaptic drive and hyperexcitability of vBNST neurons; in contrast, there was a net inhibition of the CeA. This study reveals extensive effects of chronic ethanol exposure on the basal function of cortico-limbic brain regions, suggests that there may be complex interactions between these regions in the regulation of ethanol-dependent alterations in anxiety state, and highlights the need for future examination of projection-specific effects of ethanol in cortico-limbic circuitry.

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Similar Ethanol Drinking in Adolescent and Adult C57BL/6J Mice After Chronic Ethanol Exposure and Withdrawal

Cited by 17 publications

References 52 publications

Binge ethanol withdrawal: Effects on post-withdrawal ethanol intake, glutamate–glutamine cycle and monoamine tissue content in P rat model

Binge ethanol withdrawal: Effects on post-withdrawal ethanol intake, glutamate–glutamine cycle and monoamine tissue content in P rat model

Sex differences in the behavioral sequelae of chronic ethanol exposure

Effects of chronic ethanol exposure on neuronal function in the prefrontal cortex and extended amygdala

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