Intermittent voluntary ethanol consumption combined with ethanol vapor exposure during adolescence increases drinking and alters other behaviors in adulthood in female and male rats

Amodeo, Leslie R.; Wills, Derek N.; Sanchez‐Alavez, Manuel; Nguyen, William; Conti, Bruno; Ehlers, Cindy L.

doi:10.1016/j.alcohol.2018.04.003

Cited by 64 publications

(45 citation statements)

References 73 publications

(85 reference statements)

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“…Our results are partly consistent with other studies showing that AAE induces anxiety-like disorders in adult rats (25)(26)(27) and mice (45,46). However, those results are in opposition with other findings reporting that exposure to ethanol vapor increases exploration of adult rats in the open arms of the EPM (28)(29)(30)47). OF and EPM are tasks assessing the balance between the innate exploratory drive and the anxiety generated by a novel environment (48).…”

Section: Aae Induces Anxiety-like and Depressive-like Behaviors In Adsupporting

confidence: 90%

“…AAE has been reported to promote alcohol consumption in adulthood (14, 26, 47, 49, 56), although some studies showed opposite results (57)(58)(59). Most of those studies have used rats to assess the consequences of AAE on alcohol seeking and drinking behaviors (26,30,47,60). In the present study, we confirmed that voluntary alcohol intake during adolescence promotes alcohol consumption and preference in adult male and female mice.…”

Section: Aae Enhances Adult But Not Adolescent Alcohol Consumption Ansupporting

confidence: 86%

“…Studies have suggested that repeated alcohol exposure in adolescent rats may lead to the development of anxiety-like behaviors (25)(26)(27), while other groups have showed AAE-dependent increased impulsivity in rat models (28)(29)(30). AAE-and water-exposed adolescent (P42) and adult (P80) mice underwent the Open Field (OF) and the Elevated Plus Maze (EPM) tests, which are commonly used to assess anxiety-like behaviors in rodents ( Fig 2B) (31)(32)(33).…”

Section: Adolescent Alcohol Exposure Increases Anxiety-like Behaviorsmentioning

confidence: 99%

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Adolescent alcohol binge-drinking induces delayed appearance of behavioral defects in mice

Hees

Didone

Charlet-Briar

et al. 2020

Preprint

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Adolescence is a developmental period characterized by significant changes in brain architecture and behaviors. The immaturity of the adolescent brain is associated with heightened vulnerability to exogenous agents, including alcohol. Alcohol is the most consumed drug among teenagers, and binge-drinking during adolescence is a major public health concern. Studies have suggested that, by interfering with brain maturation, adolescent alcohol exposure (AAE) may have profound and long-lasting behavioral consequences. In this study, we used an AAE model, in which adolescent male and female mice reach high blood alcohol concentration after voluntarily binge-drinking. In order to assess the short- and long-term consequences of AAE, a battery of behavioral tests was performed during late adolescence and adulthood. We showed that AAE had no short-term effect on young mice behaviors but rather increased anxiety- and depressive-like behaviors, as well as alcohol consumption during adulthood. Moreover, alcohol binge-drinking during adolescence dramatically decreased recognition memory performances and behavioral flexibility in both adult males and females. Our data suggest that AAE insidiously impairs adult behaviors, without any warning sign in late adolescence.

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Section: Aae Induces Anxiety-like and Depressive-like Behaviors In Adsupporting

confidence: 90%

Section: Aae Enhances Adult But Not Adolescent Alcohol Consumption Ansupporting

confidence: 86%

Section: Adolescent Alcohol Exposure Increases Anxiety-like Behaviorsmentioning

confidence: 99%

See 1 more Smart Citation

Adolescent alcohol binge-drinking induces delayed appearance of behavioral defects in mice

Hees

Didone

Charlet-Briar

et al. 2020

Preprint

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“…injection (Pandey et al., ), or via a combination of self‐administration and vapor exposure (Criado and Ehlers, ). Similarly, a combined vapor/self‐administration AIE exposure (intermittent pattern of vapor exposure via voluntary drinking 20% unsweetened alcohol in male and female Wistar rats P22 to 62) increased adult EtOH consumption in both sexes, with females drinking more than males (Amodeo et al., ). Further, individual rats that consumed more EtOH during adolescence (high responders) showed the largest AIE‐induced increases in alcohol drinking in adulthood (Amodeo et al., ).…”

Section: Persistent Aie‐induced Effects On Behaviormentioning

confidence: 97%

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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120

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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“…Adolescence is also a period of significant cortical modification (Gogtay et al, ) that coincides with increases in vulnerability to the effects of excessive alcohol exposure on behavior and memory (Hermens and Lagopoulos, ). We have shown, using an alcohol vapor exposure model, that alcohol exposure during adolescence can lead to deficits in several physiological and behavioral responses in rats that persist into adulthood (Amodeo et al, ; Ehlers et al, ; Ehlers et al, ). We have also shown, in young adult humans and in rats, that alcohol exposure during adolescence can cause a delay in the development of age‐associated increases in cortical connectivity (Ehlers et al, ).…”

mentioning

confidence: 99%

Time Course of Blood and Brain Cytokine/Chemokine Levels Following Adolescent Alcohol Exposure and Withdrawal in Rats

Sanchez‐Alavez

Nguyen

Mori

et al. 2019

Alcoholism Clin & Exp Res

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Background: Adolescence is a critical period for neural development, and alcohol exposure during adolescence can lead to an elevated risk for health consequences as well as alcohol use disorders. Clinical and experimental data suggest that chronic alcohol exposure may produce immunomodulatory effects that can lead to the activation of pro-inflammatory cytokine pathways as well as microglial markers. The present study evaluated, in brain and blood, the effects of adolescent alcohol exposure and withdrawal on microglia and on the most representative pro-and anti-inflammatory cytokines and major chemokines that can contribute to the establishing of a neuroinflammatory environment.Methods: Wistar rats (males, n = 96) were exposed to ethanol (EtOH) vapors, or air control, for 5 weeks over adolescence (PD22-PD58). Brains and blood samples were collected at 3 time points: (i) after 35 days of vapor/air exposure (PD58); (ii) after 1 day of withdrawal (PD59), and (iii) 28 days after withdrawal (PD86). The ionized calcium-binding adapter molecule 1 (Iba-1) was used to index microglial activation, and cytokine/chemokine responses were analyzed using magnetic bead panels.Results: After 35 days of adolescent vapor exposure, a significant increase in Iba-1 immunoreactivity was seen in amygdala, frontal cortex, hippocampus, and substantia nigra. However, Iba-1 density returned to control levels at both 1 day and 28 days of withdrawal except in the hippocampus where Iba-1 density was significantly lower than controls. In serum, adolescent EtOH exposure induced a reduction in IL-13 and an increase in fractalkine at day 35. After 1 day of withdrawal, IL-18 was reduced, and IP-10 was elevated, whereas both IP-10 and IL-10 were elevated at 28 days following withdrawal. In the frontal cortex, adolescent EtOH exposure induced an increase in IL-1b at day 35, and 28 days of withdrawal, and IL-10 was increased after 28 days of withdrawal.Conclusion: These data demonstrate that EtOH exposure during adolescence produces significant microglial activation; however, inflammatory markers seen in the blood appear to differ from those observed in the brain.

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Intermittent voluntary ethanol consumption combined with ethanol vapor exposure during adolescence increases drinking and alters other behaviors in adulthood in female and male rats

Cited by 64 publications

References 73 publications

Adolescent alcohol binge-drinking induces delayed appearance of behavioral defects in mice

Adolescent alcohol binge-drinking induces delayed appearance of behavioral defects in mice

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

Time Course of Blood and Brain Cytokine/Chemokine Levels Following Adolescent Alcohol Exposure and Withdrawal in Rats

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