Adolescent Vulnerabilities to Chronic Alcohol or Nicotine Exposure: Findings From Rodent Models

Psychology Department, University of Kentucky, Lexington, KY 40506-0044, USA.
Alcoholism Clinical and Experimental Research (Impact Factor: 3.21). 10/2005; 29(9):1720-5. DOI: 10.1097/01.alc.0000179220.79356.e5
Source: PubMed


This article presents an overview of the proceedings from a symposium entitled "Is adolescence special? Possible age-related vulnerabilities to chronic alcohol or nicotine exposure," organized by Susan Barron and Linda Spear and held at the 2004 Research Society on Alcoholism Meeting in Vancouver, British Columbia. This symposium, co-sponsored by the Fetal Alcohol Syndrome Study Group and the Neurobehavioral Teratology Society, focused on our current knowledge regarding the long-term consequences of ethanol and/or nicotine exposure during adolescence with the emphasis on data from rodent models. The support from these two societies represents the understanding by these research groups that adolescence represents a unique developmental stage for the effects of chronic drug exposure and also marks an age in which many risky behaviors including alcohol consumption and smoking typically begin. The speakers included (1) Aaron White, who presented data on the effects of adolescent ethanol exposure on subsequent motor or cognitive response to an ethanol challenge in adulthood; (2) Richard Bell, who presented data suggesting that genetic differences could play a role in adolescent vulnerability to ethanol; (3) Craig Slawecki, who presented data looking at the effects of chronic exposure to alcohol or nicotine on neurophysiologic and behavioral end points; and (4) Ed Levin, who presented data on acute and long-term consequences of adolescent nicotine exposure. Finally, Linda Spear provided some summary points and recommendations regarding unresolved issues and future directions.

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    • "This may predispose the adolescent to greater impulsivity and risk-taking, and increase the probability of drug experimentation (Spear, 2000; Chambers et al., 2003; Kuhn et al., 2013). Earlier behavioral studies using locomotor sensitization, conditioned place preference and self-administration paradigms , indicated that adolescents are more vulnerable to the detrimental effects, as well as to the rewarding and reinforcing properties, of addictive drugs (see reviews by Tirelli et al., 2003; Leslie et al., 2004; Barron et al., 2005). Increased vulnerability to cocaine reward during adolescence was recently further supported in an electrophysiological study by Wong et al. (2013), where reward unbalance in this stage is associated with heightened activity of the dopaminergic neurons. "
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    ABSTRACT: Adolescents display increased vulnerability to engage in drug experimentation. This is often considered a risk factor for later drug abuse. In this scenario, the permanent effects of cocaine exposure during adolescence on anxiety levels and stress responsivity, which may result in behavioral phenotypes prone to addiction, are now starting to be unveiled. Thus, the purpose of the present study was to evaluate the long-lasting effects of chronic cocaine administration during adolescence, on anxiety-like behavior and on stress response. Adolescent male Wistar rats were daily-administered 45 mg cocaine/kg of body weight in 3 equal intraperitoneal doses with 1h interval, from postnatal day 35 to 50. The effects of cocaine administration on anxiety levels, assessed in the Elevated Plus Maze (EPM), and on social stress response, assessed in the Resident-Intruder paradigm, were evaluated 10 days after withdrawal, when rats were reaching the adulthood. The underlying dopaminergic activity, and the corticosterone and testosterone levels were determined. Our results showed that cocaine induced long-lasting alterations in the HPA axis function and in testosterone levels. Such alterations resulted in significant and enduring changes in behavioral responses to environment challenges, such as the EPM and R/I, including the evaluation of potential threats that may lead to high-risk behavior and low benefit choices. This was further supported by an altered dopaminergic function in the amygdala and hippocampus. The present findings provide new insights into how the use of cocaine during adolescent development may modulate emotional behavior later in life. Compromised ability to recognize and deal with potential threats is an important risk factor to perpetuate compulsive drug seeking and relapse susceptibility.
    Neuroscience 07/2014; 277. DOI:10.1016/j.neuroscience.2014.07.008 · 3.36 Impact Factor
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    • "Chronic alcohol use has been shown to cause detrimental effects on cognitive processing and prefrontal cortex functioning in adolescent animals [15], [16], [17], [18]. Studies have shown that the forebrain regions in adolescent rats are especially sensitive to alcohol-induced neurodegeneration and inhibition of neurogenesis [19], [20]. "
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    ABSTRACT: Alcohol use is common in adolescence, with a large portion of intake occurring during episodes of binging. This pattern of alcohol consumption coincides with a critical period for neurocognitive development and may impact decision-making and reward processing. Prior studies have demonstrated alterations in adult decision-making following adolescent usage, but it remains to be seen if these alterations exist in adolescence, or are latent until adulthood. Here, using a translational model of voluntary binge alcohol consumption in adolescents, we assess the impact of alcohol intake on risk preference and behavioral flexibility during adolescence. During adolescence (postnatal day 30-50), rats were given 1-hour access to either a 10% alcohol gelatin mixture (EtOH) or a calorie equivalent gelatin (Control) at the onset of the dark cycle. EtOH consuming rats were classified as either High or Low consumers based on intake levels. Adolescent rats underwent behavioral testing once a day, with one group performing a risk preference task, and a second group performing a reversal-learning task during the 20-day period of gelatin access. EtOH-High rats showed increases in risk preference compared to Control rats, but not EtOH-Low animals. However, adolescent rats did a poor job of matching their behavior to optimize outcomes, suggesting that adolescents may adopt a response bias. In addition, adolescent ethanol exposure did not affect the animals' ability to flexibly adapt behavior to changing reward contingencies during reversal learning. These data support the view that adolescent alcohol consumption can have short-term detrimental effects on risk-taking when examined during adolescence, which does not seem to be attributable to an inability to flexibly encode reward contingencies on behavioral responses.
    PLoS ONE 07/2014; 9(7):e100697. DOI:10.1371/journal.pone.0100697 · 3.23 Impact Factor
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    • "studies showed that (1) the adolescent brain is in a critical period of development and is particularly sensitive to alcohol (Barron et al., 2005; Ehlers and Criado, 2010); and (2) binge drinking, characterised by the rapid alternation of intoxication and abstinence, leads to multiple withdrawals that are particularly deleterious for the brain (Obernier et al., 2002; Pascual et al., 2007). Despite these arguments suggesting that binge-drinking habits should lead to negative brain effects, very few studies explored cerebral structure or functioning in this population. "
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    ABSTRACT: Binge drinking is a major health concern, but its cerebral correlates are still largely unexplored. We aimed at exploring (1) the cognitive step at which these deficits appear and (2) the respective influence of global alcohol intake and specific binge-drinking consumption pattern on this deficit. On the basis of a screening phase (593 students), 80 participants were selected and distributed in four groups (control non-drinkers, daily drinkers, low and high binge drinkers). Event-related potentials (ERPs) were recorded while performing a simple visual oddball task. Binge drinking was associated with massive ERP impairments, starting at the perceptive level (P100/N100 and N170/P2) and spreading through the attentional (N2b/P3a) and decisional (P3b) ones. Moreover, these deficits were linked with global alcohol intake and also with the specific binge-drinking consumption pattern. Binge drinkers presented early and global ERP deficits, affecting basic and high-level cognitive stages. Moreover, we showed that binge drinking is deleterious for the brain because of alcohol consumption per se, and also because of its specific consumption pattern. The present results show that binge-drinking habits lead to striking brain consequences, particularly because of the repeated alternation between intense intoxications and withdrawal episodes.
    Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology 11/2011; 123(5):892-901. DOI:10.1016/j.clinph.2011.09.018 · 3.10 Impact Factor
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