Binge-Like, Naloxone-Sensitive, Voluntary Ethanol Intake at Adolescence Is Greater Than at Adulthood, but Does Not Exacerbate Subsequent Two-Bottle Choice Drinking

Abstract

The present study assessed the effects of ethanol exposure during adolescence or adulthood. We exposed Wistar rats, males or females, to self-administered 8-10% (v/v) ethanol (BINGE group) during the first 2 h of the dark cycle, three times a week (Monday, Wednesday, and Friday) during postnatal days (PDs) 32-54 or 72-94 (adolescent and adults, respectively). During this period, controls were only handled, and a third (IP) condition was given ethanol intraperitoneal administrations, three times a week (Monday, Wednesday, and Friday), at doses that matched those self-administered by the BINGE group. The rats were tested for ethanol intake and preference in a two-bottle (24 h long) choice test, shortly before (PD 30 or 70) and shortly after (PD 56 or 96) exposure to the binge or intraperitoneal protocol; and then tested for free-choice drinking during late adulthood (PDs 120-139) in intermittent two-bottle intake tests. Binge drinking was significantly greater in adolescents vs. adults, and was blocked by naloxone (5.0 mg/kg) administered immediately before the binge session. Mean blood ethanol levels (mg/dl) at termination of binge session 3 were 60.82 ± 22.39. Ethanol exposure at adolescence, but not at adulthood, significantly reduced exploration of an open field-like chamber and significantly increased shelter-seeking behavior in the multivariate concentric square field. The rats that had been initially exposed to ethanol at adolescence drank, during the intake tests conducted at adulthood, significantly more than those that had their first experience with ethanol at adulthood, an effect that was similar among BINGE, IP and control groups. The study indicates that binge ethanol drinking is greater in adolescent that in adults and is associated with heightened ethanol intake at adulthood. Preventing alcohol access to adolescents should reduce the likelihood of problematic alcohol use or alcohol-related consequences.

Adolescent intermittent ethanol exposure induces sex‐dependent divergent changes in ethanol drinking and motor activity in adulthood in C57BL/6J mice

“…In the present work, we exposed mice to intermittent air or ethanol exposure at the same age during adolescence and the length of abstinence was varied to allow us to understand the impact of short-term and protracted abstinence on subsequent ethanol consumption and open field behavior. This is similar to recent work that used a DID exposure paradigm and varied the withdrawal period to assess changes in ethanol consumption and anxiety-like behavior (Jimenez Chavez et al, 2020;Salguero et al, 2020). Specifically, we exposed adolescent (PND 28-42) C57BL/6J mice to adolescent intermittent ethanol (AIE) vapor exposure and measured voluntary ethanol intake (a) 1 week following the initial exposure while the mice were still adolescents and (b) 4 weeks following the AIE exposure when the mice were emerging adults.…”

Voluntary alcohol binge‐drinking in adolescent C57Bl6 mice induces delayed appearance of behavioural defects in both males and females

“…AAE has also been reported to promote alcohol consumption in adult rats, 11,36,39,47,48 although opposite results have been reported 53,54 . In the present study, voluntary adolescent binge‐drinking promoted alcohol consumption and preference in adult males and females but not in adolescents.…”

From binge eating to binge drinking: A new and robust paradigm for assessing binge ethanol self‐administration in male rats

“…A large body of evidence supports the mediating role of opioid receptors on ethanol intake, and the antagonism of this system is a common therapeutic target on AUD treatment. 24,25,29 Recent studies have reported a similar role of opioid receptors antagonism on BE as well. 30 Furthermore, both ethanol intake and BE have been reduced by modulating other pharmacological targets such as corticotropin-releasing factor, 31,32 dopamine receptors 33,34 and sigma-1 receptor, 35,36 which support the connection between the two behaviours.…”