Adolescent alcohol exposure alters the central brain circuits known to regulate the stress response

Allen, Camryn D.; Rivier, Catherine; Lee, Soon Y.

doi:10.1016/j.neuroscience.2011.03.003

Cited by 39 publications

(46 citation statements)

References 58 publications

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“…Specifically, CRF administration induces ICSS threshold elevations (Macey et al, 2000) and threshold elevations during ethanol withdrawal are reduced by a CRF antagonist (Bruijnzeel et al, 2010). Notably, adolescent ethanol exposure attenuates the adult CRF response to ethanol (Allen et al, 2011). A blunted CRF ethanol response may partly explain the diminished threshold elevations in response to acute ethanol and ethanol withdrawal (“hangover”) in AIE-exposed rats in the present study.…”

Section: Discussionmentioning

confidence: 99%

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Boutros

Semenova

Markou

2014

European Neuropsychopharmacology

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Adolescent alcohol use may interfere with neurodevelopment, increasing the likelihood of adult alcohol use disorders (AUDs). We investigated whether adolescent intermittent ethanol (AIE) exposure alters the adult reward response to ethanol. Adolescent rats were administered ethanol once (moderate exposure; Cohort 1) or three times per day (severe exposure; Cohort 2) in a 2 days on/2 days off pattern. In adulthood, subjects responded for electrical stimulation directed at the posterior lateral hypothalamus in a discrete-trials intracranial self-stimulation (ICSS) procedure that provides current-intensity thresholds as a measure of brain reward function. The effects of ethanol administration and withdrawal were assessed. Control rats showed dose-dependent threshold elevations after acute ethanol, indicating reward deficits. A majority of moderately AIE-exposed rats (Cohort 1) showed threshold lowering after ethanol, suggesting ethanol-induced reward enhancement in this sub-set of rats. Rats exposed to severe AIE (Cohort 2) showed no threshold elevation or lowering, suggesting blunted affective ethanol response. Daily ethanol induced threshold elevations 24 h after administration in control but not in either group of AIE-exposed rats, suggesting decreased sensitivity to the negative affective state of ethanol withdrawal. Withdrawal from a 4-day ethanol binge produced robust and enduring threshold elevations in all rats, although threshold elevations were diminished in rats exposed to severe AIE. These results indicate that AIE exposure diminished reward deficits associated with ethanol intoxication and withdrawal and may have increased ethanol-induced reward enhancement in a sub-set of rats. In humans, enhanced ethanol reward accompanied by reduced withdrawal severity may contribute to the development of AUDs.

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Section: Discussionmentioning

confidence: 99%

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Boutros

Semenova

Markou

2014

European Neuropsychopharmacology

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“…Alcohol exposure is known to attenuate the HPA response to stress [51]. Furthermore, blunted HPA axis responses to stress have been reported after adolescent ethanol exposure [31,32]. In the present studies, AIE exposure increased CRF mRNA levels in the CeA regardless of stress exposure, although the effect appeared to be more pronounced in non-stressed AIE-exposed rats (post hoc comparisons were not performed because there was no significant AIE × Stress interaction effect in the ANOVA).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the use of vapor exposure limits the potentially confounding effects of stress experienced during AIE exposure on risky choice under baseline conditions and in response to stress during adulthood. We showed previously that the AIE vapor exposure used in the present studies altered the adult CRF system in the hypothalamic-pituitary-adrenal axis that regulates the stress response [31,32]. Therefore, we also investigated the effects of acute and chronic social defeat stress in AIE vapor- and air-exposed rats.…”

Section: Introductionmentioning

confidence: 88%

Risky choice and brain CRF after adolescent ethanol vapor exposure and social stress in adulthood

Boutros

Der-Avakian

Semenova

et al. 2016

Behavioural Brain Research

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Adolescent ethanol exposure increases risky choice and alters corticotropin releasing factor (CRF) systems in adulthood. The impact of stress on risky choice after adolescent intermittent ethanol (AIE) exposure is not known. We investigated time-specific effects of AIE vapor exposure during early adolescence on risky choice after stress or no stress in adulthood. Male Wistar rats were exposed to air or AIE vapor on postnatal days 28–42 (adolescence) and were exposed to 10 days of social defeat or no stress on postnatal days 172–181 (adulthood). Risky choice was assessed in the probability discounting task under baseline conditions and after days 1 and 10 of social defeat. CRF and CRF receptor 1 (CRFR1) mRNA levels were assessed in the prefrontal cortex (PFC) and the central nucleus of the amygdala (CeA) 24 h post-stress to evaluate persistent effects of stress on the brain. AIE exposure had no effect on risky choice either at baseline or after social defeat. Additionally, neither acute nor chronic social defeat affected risky choice in air-exposed rats. In the PFC, chronic social defeat selectively decreased CRF mRNA levels in air-exposed rats and increased CRFR1 mRNA levels in all rats. AIE exposure increased CRF mRNA levels in the CeA with no effect of social stress. Our results indicate no effect of ethanol exposure via vapor during early adolescence on risky choice, while our previous findings indicated that AIE exposure via gavage affected risky choice. Both AIE exposure and social defeat altered CRF and CRFR1 mRNA levels in the brain.

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“…All sections were maintained in an antifreeze solution (50% 0.1 M phosphate buffered saline, 20% glycerol, 30% ethylene glycol) at −20°C until analysis. Briefly, double DAB immunohistochemistry (IHC) staining was performed on free-floating sections as described previously (Choi et al, 2008, Allen et al, 2011b) with a rabbit anti-c-fos antibody (1:10,000, Calbiochem, San Diego, CA, USA) stained black and a sheep anti-PNMT antibody (1:7500, Chemicon/Millipore, Billerica, MA, USA) stained brown. Sections were mounted on gelatin-coated sub slides, dehydrated, and coverslipped using DPX mounting medium (Electron Microscopy Sciences, Hatfield, PA).…”

Section: Methodsmentioning

confidence: 99%

“…In adolescent self-administering binge-drinking animals, we found a decrease in the number of Crf cells in the young adult amygdala (Allen et al, 2011a), a brain region that is important in conveying the emotional component of the stress response (Pich et al, 1995). Additionally, we have shown that AIE exerts long-term effects on the ability of the PVN to respond to an alcohol challenge in young adulthood, possibly mediated by catecholaminergic input from the brain stem to the PVN as seen by changes in activation (measured via c-fos immunoreactivity) of phenylethanolamine N-methyltransferase (PNMT) neurons (Allen et al, 2011b, Logrip et al, 2013). These results prompted us to investigate whether AIE exposure similarly or differentially affects the response to a distinct acute stressor, an alcohol challenge in young adult and adult male rats.…”

Section: Introductionmentioning

confidence: 99%

Exposure to alcohol during adolescence exerts long-term effects on stress response and the adult brain stress circuits

et al. 2016

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The hypothalamic-pituitary-adrenal (HPA) axis undergoes critical developments during adolescence. Therefore, stressors experienced during this period potentially have long-term effects on adult HPA axis function. We hypothesized that adolescent intermittent ethanol (AIE) exposure would affect adult HPA axis function, resulting in altered responses to an alcohol challenge in young adults or adults. To test these hypotheses, male rats were exposed to alcohol vapor for 6 h per day from post-natal day (PND) 28–42, then acutely challenged with alcohol intragastrically (3.2–4.5 g/kg) in young adults (PND 70) or adults (PND 90). Overall, we observed blunted HPA axis responses to an alcohol challenge due to AIE exposure. Specifically, AIE tended to inhibit the alcohol-challenge-induced increase in plasma corticosterone (CORT) concentrations in young adult and adult rats. As well, AIE significantly blunted the alcohol challenge-induced arginine vasopressin (Avp) mRNA expression in the paraventricular nucleus (PVN) of the hypothalamus of adult rats. Results of the present study are similar to what we have previously shown, that these changes in PVN responsiveness may result from AIE-induced alterations in adrenergic neurons in brain stem regions C1–C3 known to project to the PVN. AIE elevated the number of colocalized c-fos/phenylethanolamine N-methyltransferase (PNMT)-positive cell bodies in the C1 region of adult rats. Together, this data suggests that AIE exposure produces alterations in male HPA axis responsiveness to administration of an acute alcohol challenge that may be long-lasting.

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Adolescent alcohol exposure alters the central brain circuits known to regulate the stress response

Cited by 39 publications

References 58 publications

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Adolescent intermittent ethanol exposure diminishes anhedonia during ethanol withdrawal in adulthood

Risky choice and brain CRF after adolescent ethanol vapor exposure and social stress in adulthood

Exposure to alcohol during adolescence exerts long-term effects on stress response and the adult brain stress circuits

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