The reinforcing properties of ethanol are quantitatively enhanced in adulthood by peri-adolescent ethanol, but not saccharin, consumption in female alcohol-preferring (P) rats

Toalston, Jamie E.; Deehan, Gerald A.; Hauser, Sheketha R.; Engleman, Eric A.; Bell, Richard L.; Murphy, James M.; McBride, William J.; Rodd, Zachary A.

doi:10.1016/j.alcohol.2015.04.007

Cited by 21 publications

(13 citation statements)

References 37 publications

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“…Alcohol consumption in rodents is known to vary by species, strain, method, and environment (Crabbe et al., ; Fritz and Boehm, ). Nevertheless, the majority of rodent studies, including those from the NADIA Consortium, report that AIE often, although not always (Moaddab et al., ; Nentwig et al., ; Toalston et al., ; Varlinskaya et al., ), promotes adult alcohol drinking in multiple rat strains (Alaux‐Cantin et al., ; Broadwater et al., ; Gass et al., ; Lee et al., ; Pandey et al., ; Pascual et al., ; Rodd‐Henricks et al., ; Toalston et al., ; Wille‐Bille et al., ). These studies use a variety of AIE exposures as well as alcohol consumption paradigms.…”

Section: Persistent Aie‐induced Effects On Behaviormentioning

confidence: 99%

Mechanisms of Persistent Neurobiological Changes Following Adolescent Alcohol Exposure: NADIA Consortium Findings

Crews

Robinson

Chandler³

et al. 2019

Alcoholism Clin & Exp Res

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125

153

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The Neurobiology of Adolescent Drinking in Adulthood (NADIA) Consortium has focused on the impact of adolescent binge drinking on brain development, particularly on effects that persist into adulthood. Adolescent binge drinking is common, and while many factors contribute to human brain development and alcohol use during adolescence, animal models are critical for understanding the specific consequences of alcohol exposure during this developmental period and the underlying mechanisms. Using adolescent intermittent ethanol (AIE) exposure models, NADIA investigators identified long‐lasting AIE‐induced changes in adult behavior that are consistent with observations in humans, such as increased alcohol drinking, increased anxiety (particularly social anxiety), increased impulsivity, reduced behavioral flexibility, impaired memory, disrupted sleep, and altered responses to alcohol. These behavioral changes are associated with multiple molecular, cellular, and physiological alterations in the brain that persist long after AIE exposure. At the molecular level, AIE results in long‐lasting changes in neuroimmune/trophic factor balance and epigenetic–microRNA (miRNA) signaling across glia and neurons. At the cellular level, AIE history is associated in adulthood with reduced expression of cholinergic, serotonergic, and dopaminergic neuron markers, attenuated cortical thickness, decreased neurogenesis, and altered dendritic spine and glial morphology. This constellation of molecular and cellular adaptations to AIE likely contributes to observed alterations in neurophysiology, measured by synaptic physiology, EEG patterns, and functional connectivity. Many of these AIE‐induced brain changes replicate findings seen in postmortem brains of humans with alcohol use disorder (AUD). NADIA researchers are now elucidating mechanisms of these adaptations. Emerging data demonstrate that exercise, antiinflammatory drugs, anticholinesterases, histone deacetylase inhibitors, and other pharmacological compounds are able to prevent (administered during AIE) and/or reverse (given after AIE) AIE‐induced pathology in adulthood. These studies support hypotheses that adolescent binge drinking increases risk of adult hazardous drinking and influences brain development, and may provide insight into novel therapeutic targets for AIE‐induced neuropathology and AUDs.

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Section: Persistent Aie‐induced Effects On Behaviormentioning

confidence: 99%

Mechanisms of Persistent Neurobiological Changes Following Adolescent Alcohol Exposure: NADIA Consortium Findings

Crews

Robinson

Chandler³

et al. 2019

Alcoholism Clin & Exp Res

Self Cite

125

153

View full text Add to dashboard Cite

show abstract

“…Studies using animal models have also indicated that voluntary ethanol drinking during adolescence can, in some models, be shown to facilitate the acquisition of alcohol self-administration, increase craving behavior, and/or increase the probability of relapse in those animals in adulthood (see Alaux-Cantin et al, 2013; Gilpin, Karanikas & Richardson, 2012; Jeanblanc et al, 2015; McBride et al, 2005; Serlin & Torregrossa, 2015; Spear, 2000a; Toalston et al, 2015). However, other studies have shown that ethanol exposure during adolescence has no effect on subsequent ethanol consumption in adulthood (Slawecki & Betancourt, 2002).…”

Section: Introductionmentioning

confidence: 99%

Alcohol drinking during adolescence increases consumptive responses to alcohol in adulthood in Wistar rats

Amodeo

Kneiber

Wills

et al. 2017

Alcohol

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Binge drinking and the onset of alcohol use disorders usually peak during the transition between late adolescence and early adulthood, and early adolescent onset of alcohol consumption has been demonstrated to increase the risk for alcohol dependence in adulthood. In the present study we describe an animal model of early adolescent alcohol consumption where animals drink unsweetened and unflavored ethanol in high concentrations (20%). Using this model we investigated the influence of drinking on alcohol-related appetitive behavior and alcohol consumption levels in early adulthood. Further, we also sought to investigate whether differences in alcohol-related drinking behaviors were specific to exposure in adolescence versus exposure in adulthood. Male Wistar rats were given a 2-bottle choice between 20% ethanol and water in one group and between two water bottles in another group during their adolescence (Postnatal Day (PD) PD26-59) to model voluntary drinking in adolescent humans. As young adults (PD85), rats were trained in a paradigm that provided free access to 20% alcohol for 25 min after completing up to a fixed ratio (FR) 16-lever press response. A set of young adult male Wistar rats was exposed to the same paradigm using the same time course beginning at PD92. The results indicate that adolescent exposure to alcohol increased consumption of alcohol in adulthood. Furthermore, when investigating differences between adolescent high and low adolescent drinkers in adulthood, high consumers continued to drink more alcohol, had fewer FR failures, and had faster completion of FR schedules in adulthood whereas the low consumers were no different than controls. Rats exposed to ethanol in young adulthood also increased future intake but there were no differences in any other components of drinking behavior. Both adolescent- and adult-exposed rats did not exhibit an increase in lever pressing during the appetitive challenge session. These data indicate that adolescent and early adult alcohol exposure can increase consumptive aspects of drinking but that adolescent exposure may preferentially influence the motivation to drink.

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“…In contrast to the causal ambiguity in human studies, longitudinal preclinical studies allow scientists to isolate the effects of adolescent alcohol exposure on behavior and neurobiology in adulthood (Crews et al., ). To date, such studies have shown that adolescent intermittent ethanol (AIE) exposure leads to impaired reversal learning (Coleman et al., ), enhanced cue‐driven behavior (McClory and Spear, ), increased ethanol (EtOH)‐induced conditioned place preference (Pascual et al., ), greater EtOH self‐administration (Pascual et al., ; Toalston et al., ; but see Slawecki and Betancourt, ), and resistance to extinction of EtOH self‐administration (Gass et al., ; Toalston et al., ).…”

mentioning

confidence: 99%

Sex and Adolescent Ethanol Exposure Influence Pavlovian Conditioned Approach

Madayag

Stringfield

Reissner

et al. 2017

Alcoholism Clin & Exp Res

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BACKGROUND Alcohol use among adolescents is widespread and a growing concern due to long-term behavioral deficits, including altered Pavlovian behavior, that potentially contribute to addiction vulnerability. We tested the hypothesis that adolescent intermittent ethanol (AIE) exposure alters Pavlovian behavior in males and females as measured by a shift from goal-tracking to sign-tracking. Additionally, we investigated GLT-1, an astrocytic glutamate transporter, as a potential contributor to a sign-tracking phenotype. METHODS Male and female Sprague-Dawley rats were exposed to AIE (5g/Kg, intragastric) or water intermittently 2 days on, 2 days off from postnatal day (P) 25 to 54. Around P70, animals began 20 daily sessions of Pavlovian conditioned approach, where they learned that a cue predicted non-contingent reward delivery. Lever pressing indicated interaction with the cue, or sign-tracking, and receptacle entries indicated approach to the reward delivery location, or goal-tracking. To test for effects of AIE on nucleus accumbens excitatory signaling, we isolated membrane subfractions and measured protein levels of the glutamate transporter GLT-1 after animals completed behavior as a measure of glutamate homeostasis. RESULTS Females exhibited elevated sign-tracking compared to males with significantly more lever presses, faster latency to first lever press, and greater probability to lever press in a trial. AIE significantly increased lever pressing while blunting goal tracking, as indicated by fewer cue-evoked receptacle entries, slower latency to receptacle entry, and lower probability to enter the receptacle in a trial. No significant Sex-by-Exposure interactions were observed in sign- or goal-tracking metrics. Moreover, we found no significant effects of Sex or Exposure on membrane GLT-1 expression in the nucleus accumbens. CONCLUSIONS Females exhibited enhanced sign-tracking compared to males, while AIE decreased goal-tracking compared to control exposure. Our findings support the hypothesis that adolescent binge ethanol can shift conditioned behavior from goal- to cue-directed in Pavlovian conditioned approach, especially in females.

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The reinforcing properties of ethanol are quantitatively enhanced in adulthood by peri-adolescent ethanol, but not saccharin, consumption in female alcohol-preferring (P) rats

Cited by 21 publications

References 37 publications

Mechanisms of Persistent Neurobiological Changes Following Adolescent Alcohol Exposure: NADIA Consortium Findings

Mechanisms of Persistent Neurobiological Changes Following Adolescent Alcohol Exposure: NADIA Consortium Findings

Alcohol drinking during adolescence increases consumptive responses to alcohol in adulthood in Wistar rats

Sex and Adolescent Ethanol Exposure Influence Pavlovian Conditioned Approach

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