Review Article | Published:

Effects of adolescent alcohol consumption on the brain and behaviour

Nature Reviews Neuroscience volume 19, pages 197214 (2018) | Download Citation

This article has been updated


Per occasion, alcohol consumption is higher in adolescents than in adults in both humans and laboratory animals, with changes in the adolescent brain probably contributing to this elevated drinking. This Review examines the contributors to and consequences of the use of alcohol in adolescents. Human adolescents with a history of alcohol use differ neurally and cognitively from other adolescents; some of these differences predate the commencement of alcohol consumption and serve as potential risk factors for later alcohol use, whereas others emerge from its use. The consequences of alcohol use in human adolescents include alterations in attention, verbal learning, visuospatial processing and memory, along with altered development of grey and white matter volumes and disrupted white matter integrity. The functional consequences of adolescent alcohol use emerging from studies of rodent models of adolescence include decreased cognitive flexibility, behavioural inefficiencies and elevations in anxiety, disinhibition, impulsivity and risk-taking. Rodent studies have also showed that adolescent alcohol use can impair neurogenesis, induce neuroinflammation and epigenetic alterations, and lead to the persistence of adolescent-like neurobehavioural phenotypes into adulthood. Although only a limited number of studies have examined comparable measures in humans and laboratory animals, the available data provide evidence for notable across-species similarities in the neural consequences of adolescent alcohol exposure, providing support for further translational efforts in this context.

Key points

  • Per occasion, alcohol use is higher among adolescents than adults in both humans and laboratory animals, suggesting that maturational changes in the adolescent brain contribute to the elevation in alcohol consumption seen at this time.

  • Human prospective studies have revealed evidence that certain neural and cognitive or personality associates of heavy adolescent alcohol use may predate and serve as risk factors for such use.

  • There is substantial evidence for notable neural and cognitive consequences of repeated exposure to alcohol during adolescence emerging from both human prospective studies and studies using rodent models. Although dependent measures often differ considerably across species, where comparable measures have been used, evidence for concordance in neural alterations has emerged across species, including disrupted myelination, poorer white matter integrity, alterations in connectivity between frontal and limbic regions and electroencephalographic changes.

  • Studies have revealed that adolescent alcohol exposure is associated with various cognitive and other functional deficits. The consequences that have emerged in human longitudinal work include deficits in verbal learning, attention, and visuospatial and memory tasks, whereas studies using animal models of adolescent alcohol exposure have revealed that such exposure is linked to decreases in cognitive flexibility, behavioural inefficiencies, increases in anxiety-like behaviour, disinhibition, elevated risk-taking, augmented later voluntary consumption and motivation for alcohol, and the persistence of adolescent-like phenotypes into adulthood.

  • In rodent studies, repeated exposure to alcohol during adolescence induces reliable and specific neural alterations that include decreases in cholinergic tone in the basal forebrain, neuroinflammation, disruptions in neurogenesis, epigenetic alterations and the persistence of certain adolescent-like neural characteristics into adulthood.

  • There are numerous critical areas for future work in this area using human longitudinal designs as well as studies in laboratory animals — work that could benefit from an increasing focus on assessment of comparable measures across species. Studies examining functional consequences of adolescent alcohol exposure have largely used different measures to date, with a focus on neuropsychological or cognitive tests in humans contrasting with an emphasis on alterations in risk-taking, anxiety, and later motivation for and sensitivity to alcohol in rodent studies.

Access optionsAccess options

Rent or Buy article

Get time limited or full article access on ReadCube.


All prices are NET prices.

Change history

  • 15 May 2018

    In the initially published version of this article, the following sentence was incorrect: "Studies that have compared equivalent exposures to alcohol in adolescent and adult animals have found that the effects of alcohol exposure during adolescence are generally not evident or are less pronounced than after comparable alcohol exposure in adulthood". The sentence should have read: "Studies that have compared equivalent exposures to alcohol in adolescent and adult animals have found that the effects of alcohol exposure during adulthood are generally not evident or are less pronounced than after comparable alcohol exposure in adolescence". The sentence has been corrected in the HTML and PDF versions of the article.


  1. 1.

    The adolescent brain and age-related behavioral manifestations. Neurosci. Biobehav. Rev., 24, 417–463 (2000).

  2. 2.

    Alcohol consumption in adolescence: a translational perspective. Curr. Addict. Rep. 3, 50–61 (2016).

  3. 3.

    et al. Monitoring the Future national survey results on drug use: 1975-2015: Overview, key findings on adolescent drug use (Institute for Social Research, The University of Michigan, 2016).

  4. 4.

    & International perspectives on adolescent and young adult drinking. Alcohol. Res. Health 28, 258–268 (2004).

  5. 5.

    , , , & Monitoring the Future national survey results on drug use, 1975-2015: Volume I, Secondary school students (Institute for Social Research, The University of Michigan, 2016).

  6. 6.

    Drinking over the lifespan: Focus on early adolescents and youth. Alcohol Res. 38, 95–101 (2016).

  7. 7.

    et al. Extreme binge drinking among 12th-grade students in the United States: prevalence and predictors. JAMA Pediatr. 167, 1019–1025 (2013). This study demonstrates the very high rates of alcohol consumption among some adolescents (>10–15 drinks per occasion).

  8. 8.

    Substance Abuse and Mental Health Services Administration. National Survey on Drug Use and Health, 2007 (2007).

  9. 9.

    , , & Factors influencing elevated ethanol consumption in adolescent relative to adult rats. Alcohol. Clin. Exp. Res. 29, 1796–1808 (2005).

  10. 10.

    et al. Pubertal status, sensation-seeking, impulsivity, and substance use in high school-aged boys and girls. J. Addict. Med. 7, 116–121 (2013).

  11. 11.

    , & Puberty and gonadal hormones: Role in adolescent-typical behavioral alterations. Horm. Behav. 64, 343–349 (2013).

  12. 12.

    Adolescent neurodevelopment. J. Adolesc. Health 52, S2–S12 (2013).

  13. 13.

    & microRNAs and the adolescent brain: filling the knowledge gap. Neurosci. Biobehav. Rev. 70, 313–322 (2016).

  14. 14.

    , & Mechanisms contributing to prefrontal cortex maturation during adolescence. Neurosci. Biobehav. Rev. 70, 4–12 (2016).

  15. 15.

    , & Braking and accelerating of the adolescent brain. J. Res. Adolesc. 21, 21–33 (2011).

  16. 16.

    Adolescent brain development in normality and psychopathology. Dev. Psychopathol. 25, 1325–1345 (2013).

  17. 17.

    , , , & An integrative model of the maturation of cognitive control. Annu. Rev. Neurosci. 38, 151–170 (2015).

  18. 18.

    & Special issue on the adolescent brain. Neurosci. Biobehav. Rev. 70, 1–3 (2016).

  19. 19.

    , & Synaptic development of the cerebral cortex: implications for learning, memory, and mental illness. Prog. Brain Res. 102, 227–243 (1994).

  20. 20.

    & Pubertal onset as a critical transition for neural development and cognition. Brain Res. 1654, 87–94 (2017).

  21. 21.

    Mapping brain maturation and cognitive development during adolescence. Trends Cogn. Sci. 9, 60–68 (2005).

  22. 22.

    The Behavioral Neuroscience of Adolescence (W. W. Norton, 2010).

  23. 23.

    The triadic model perspective for the study of adolescent motivated behavior. Brain Cogn. 89, 104–111 (2014).

  24. 24.

    Rewards, aversions and affect in adolescence: emerging convergences across laboratory animal and human data. Dev. Cogn. Neurosci. 1, 390–343 (2011).

  25. 25.

    et al. Dopamine neurons in the ventral tegmental area fire faster in adolescent rats than in adults. J. Neurophysiol. 108, 1620–1630 (2012).

  26. 26.

    & Heterogeneity of dopamine neuron activity across traits and states. Neuroscience 282, 176–197 (2014).

  27. 27.

    & Stress in adolescence and drugs of abuse in rodent models: role of dopamine, CRF, and HPA axis. Psychopharmacology 231, 1557–1580 (2014).

  28. 28.

    Rethinking schizophrenia. Nature 468, 187–193 (2010).

  29. 29.

    A role for synaptic plasticity in the adolescent development of executive function. Transl Psychiatry 3, e238 (2013).

  30. 30.

    , , & Loss of δ-GABAA receptor-mediated tonic currents in the adult prelimbic cortex following adolescent alcohol exposure. Addict. Biol. 22, 616–628 (2017).

  31. 31.

    & GABAergic function as a limiting factor for prefrontal maturation during adolescence. Trends Neurosci. 39, 441–448 (2016).

  32. 32.

    , , , & Different developmental trajectories for anticipation and receipt of reward during adolescence. Dev. Cogn. Neurosci. 6, 113–124 (2013).

  33. 33.

    & Neural processing of reward in adolescent rodents. Dev. Cogn. Neurosci. 11, 145–154 (2015).

  34. 34.

    & Reward-centricity and attenuated aversions: an adolescent phenotype emerging from studies in laboratory animals. Neurosci. Biobehav. Rev. 70, 121–134 (2016).

  35. 35.

    , , & Age differences in the impact of peers on adolescents' and adults' neural response to reward. Dev. Cogn. Neurosci. 11, 75–82 (2015).

  36. 36.

    Motivations for alcohol use among adolescents: development and validation of a four-factor model. Physiol. Assess. 6, 117–128 (1994).

  37. 37.

    , & The relations of trait anxiety, anxiety sensitivity, and sensation seeking to adolescents' motivation for alcohol, cigarette, and marijuana use. Addict. Behav. 26, 803–825 (2001).

  38. 38.

    , & Ethanol intake under social circumstances or alone in Sprague-Dawley rats: impact of age, sex, social activity, and social anxiety-like behavior. Alcohol. Clin. Exp. Res. 39, 117–125 (2015).

  39. 39.

    , & Sex differences in sensitivity to the social consequences of acute ethanol and social drinking during adolescence. Behav. Brain. Res. 282, 6–13 (2015).

  40. 40.

    & Neurobiology of the adolescent brain and behavior: implications for substance use disorders. J. Am. Acad. Child Adolesc. Psychiatry 49, 1189–1201 (2010).

  41. 41.

    et al. The dual systems model: review, reappraisal, and reaffirmation. Dev. Cogn. Neurosci. 17, 103–117 (2016).

  42. 42.

    Beyond simple models of self-control to circuit-based accounts of adolescent behavior. Annu. Rev. Psychol. 66, 295–319 (2015).

  43. 43.

    , & Beyond simple models of adolescence to an integrated circuit-based account: a commentary. Dev. Cogn. Neurosci. 17, 128–130 (2016).

  44. 44.

    , , & Adolescent alcohol exposure persistently impacts adult neurobiology and behavior. Pharmacol. Rev. 68, 1074–1109 (2016).

  45. 45.

    et al. Affective decision-making deficits, linked to a dysfunctional ventromedial prefrontal cortex, revealed in 10th grade Chinese adolescent binge drinkers. Neuropsychologia 46, 714–726 (2008).

  46. 46.

    , , , & Neuropsychological performance of South African treatment-naive adolescents with alcohol dependence. Drug Alcohol. Depend. 110, 8–14 (2010).

  47. 47.

    et al. Adolescent substance abuse: the effects of alcohol and marijuana on neuropsychological performance. Alcohol. Clin. Exp. Res. 15, 39–46 (2011).

  48. 48.

    et al. Executive functioning and alcohol binge drinking in university students. Addict. Behav. 17, 167–172 (2012).

  49. 49.

    et al. Cognitive, emotion control, and motor performance of adolescents in the NCANDA study: contributions from alcohol consumption, age, sex, ethnicity and family history of addiction. Neuropsychology,30, 449–473 (2016).

  50. 50.

    , , & Inhibition during early adolescence predicts alcohol and marijuana use by late adolescence. Neuropsychology 28, 782–790 (2014).

  51. 51.

    et al. Working memory ability predicts trajectories of early alcohol use in adolescents: the meditational role of impulsivity. Addiction 108, 506–515 (2012).

  52. 52.

    et al. Neural predictors of initiating alcohol use during adolescence. Am. J. Psychiatry 174, 172–185 (2017). This study uses a longitudinal design to reveal a number of cognitive, demographic and neural factors that serve as predictors for the subsequent initiation and escalation of alcohol use during adolescence.

  53. 53.

    et al. Prediction of alcohol drinking in adolescents: personality-traits, behavior, brain responses, and genetic variations in the context of reward sensitivity. Biol. Psychol. 118, 79–87 (2016). This paper from the IMAGEN longitudinal study provides evidence that personality traits predict the initiation of alcohol use whereas genetic factors have a greater influence on the escalation of alcohol use during adolescence.

  54. 54.

    A developmental behavior-genetic perspective on alcoholism risk. Alcohol Health Res. World 22, 131–143 (1998).

  55. 55.

    et al. Polygenic risk, personality dimensions, and adolescent alcohol use problems: a longitudinal study. J. Stud. Alcohol. Drugs 78, 442–451 (2017).

  56. 56.

    et al. Learning and memory in adolescent moderate, binge, and extreme-binge drinkers. Alcohol. Clin. Exp. Res. 40, 1895–1904 (2016).

  57. 57.

    , , & Substance use and withdrawal: neuropsychological functioning over 8 years in youth. J. Int. Neuropsychol. 8, 873–883 (2002). This longitudinal study followed individuals from mid-adolescence to emerging adulthood and found that the amount of substance use over the 8-year period was predictive of performance deficits in memory and attention tests, whereas the frequency of withdrawal symptoms was associated with other deficits such as impaired visuospatial functioning.

  58. 58.

    et al. Impact of adolescent alcohol and drug use on neuropsychological functioning in young adulthood: 10-year outcomes. J. Child. Adolesc. Subst. Abuse 20, 135–154 (2011).

  59. 59.

    et al. Binge drinking trajectory and neuropsychological functioning among university students: a longitudinal study. Drug Alcohol. Depend. 133, 108–114 (2013).

  60. 60.

    , , , & Initiating moderate to heavy alcohol use predicts changes in neuropsychological functioning for adolescent girls and boys. Psychol. Addict. Behav. 23, 715–722 (2009).

  61. 61.

    & Neurotoxic effects of alcohol in adolescence. Annu. Rev. Clin. Psychol. 9, 703–721 (2013).

  62. 62.

    , , & Neurocognitive functioning of adolescents: effects of protracted alcohol use. Alcohol. Clin. Exp. Res. 24, 164–171 (2000).

  63. 63.

    , , , & Learning and memory performances in adolescent users of alcohol and marijuana: interactive effects. J. Stud. Alcohol. Drugs 71, 885–894 (2010).

  64. 64.

    et al. Consequences of multiple withdrawals from alcohol. Alcohol. Clin. Exp. Res. 28, 233–246 (2004).

  65. 65.

    , & Exacerbation of ethanol withdrawal seizures in mice with a history of multiple withdrawal experience. Pharmacol. Biochem. Behav. 57, 179–183 (1997).

  66. 66.

    & The effects of continuous and intermittent ethanol exposure in adolescence on the aversive properties of ethanol during adulthood. Alcohol. Clin. Exp. Res. 31, 2020–2027 (2007).

  67. 67.

    , , & Effects of different ethanol-administration regimes on mRNA and protein levels of steroid 5α-reductase isozymes in prefrontal cortex of adolescent male rats. Psychopharmacoloy 231, 3273–3280 (2014).

  68. 68.

    , & Anxiogenic effects during withdrawal from acute ethanol in adolescent and adult rats. Pharmacol. Biochem. Behav. 75, 411–418 (2003).

  69. 69.

    , , & Differential dietary ethanol intake and blood ethanol levels in adolescent and adult rats: effects on anxiety-like behavior and seizure thresholds. Alcohol. Clin. Exp. Res. 32, 1350–1360 (2008).

  70. 70.

    , , & Sensitization, duration, and pharmacological blockade of anxiety-like behavior following repeated ethanol withdrawal in adolescent and adult rats. Alcohol. Clin. Exp. Res. 33, 455–463 (2009).

  71. 71.

    , , & Cognitive impairments in abstinent alcoholics. West. J. Med. 152, 531–537 (1990).

  72. 72.

    Adolescent alcohol exposure: are there separable vulnerable periods within adolescence? Phsyiol. Behav. 148, 122–130 (2015).

  73. 73.

    , , , & Acute and chronic effects of alcohol on trail making test performance among underage drinkers in a field setting. J. Stud. Alcohol Drugs 74, 635–641 (2013).

  74. 74.

    et al. Effects of acute or chronic ethanol exposure during adolescence on behavioral inhibition and efficiency in a modified water maze task. PLoS ONE 8, e77768 (2013).

  75. 75.

    Attention, impulsivity, and cognitive flexibility in adult male rats exposed to ethanol binge during adolescence as measured in the five-choice serial reaction time task: the effects of task and ethanol challenges. Psychopharmacology 219, 433–442 (2012).

  76. 76.

    , , , & Adolescent binge drinking alters adult brain neurotransmitter gene expression, behavior, brain regional volumes, and neurochemistry in mice. Alcohol. Clin. Exp. Res. 35, 671–688 (2011).

  77. 77.

    , et al. Adolescent binge ethanol treatment alters adult brain regional volumes, cortical extracellular matrix protein and behavioral flexibility. Pharmacol. Biochem. Behav. 116, 142–151 (2014).

  78. 78.

    et al. Adolescent alcohol exposure reduces behavioral flexibility, promotes disinhibition, and increases resistance to extinction of ethanol self-administration in adulthood. Neuropsychopharmacology 39, 2570–2583 (2014). This study demonstrates that alcohol exposure during adolescence decreases cognitive flexibility and increases disinhibition when rats are later tested in adulthood.

  79. 79.

    et al. Long-term effects of chronic intermittent ethanol exposure in adolescent and adult rats: radial-arm maze performance and operant food reinforced responding. PLoS ONE 8, e62940 (2013).

  80. 80.

    et al. Behavioral inefficiency on a risky decision-making task in adulthood after adolescent intermittent ethanol exposure in rats. Sci. Rep. 7, 4680 (2017).

  81. 81.

    , & Chronic intermittent ethanol during adolescence: effects on social behavior and ethanol sensitivity in adulthood. Alcohol 48, 433–444 (2014). This study demonstrates that alcohol exposure during early-mid but not mid-late adolescence increases social anxiety-like behaviour in male (but not female) adult rats and results in the persistence of adolescent-typical social facilitatory effects of ethanol into adulthood.

  82. 82.

    , & Chronic intermittent ethanol exposure during adolescence effects on stress-induced social alterations and social drinking in adulthood. Brain Res. 1654, 145–156 (2016).

  83. 83.

    , , & Potential role of adolescent alcohol exposure-induced amygdaloid histone modifications in anxiety and alcohol intake during adulthood. Neurobiol. Dis. 82, 607–619 (2015). This paper shows notable alterations in epigenetic regulation in the amygdala following adolescent alcohol exposure, with inhibition of these alterations in histone regulation attenuating the increases in anxiety and elevated alcohol intake seen in exposed animals in adulthood.

  84. 84.

    et al. A role for histone acetylation mechanisms in adolescent exposure-induced deficits in hippocampal brain-derived neurotrophic factor expression and neurogenesis markers in adulthood. Brain Struct. Funct. 221, 4691–4703 (2016). This study relates changes in epigenetic regulation (histone acetylation) to disruptions in neurogenesis and decreases in BDNF after adolescent alcohol exposure.

  85. 85.

    , , & Adolescent binge alcohol exposure increases risk assessment behaviors in male Wistar rats after exposure to an acute psychological stressor in adulthood. Psychoneuroendocrinology 76, 154–161 (2017).

  86. 86.

    , & Long-term neurobehavioral effects of alcohol or nicotine exposure in adolescent animal models. Ann. NY Acad. Sci. 1021, 448–452 (2004).

  87. 87.

    , , & Negative affect and excessive alcohol intake incubate during protracted withdrawal from binge-drinking in adolescent, but not adult, mice. Front. Psychol. 8, 1128 (2017).

  88. 88.

    , , , & Adolescent, but not adult, binge ethanol exposure leads to persistent global reductions of choline acetyltransferase expressing neurons in brain. PLoS ONE 9, e113421 (2014).

  89. 89.

    , & Adolescent binge drinking leads to changes in alcohol drinking, anxiety, and amygdalar corticotropin releasing factor cells in adulthood in male rats. PLoS ONE 7, e31466 (2012).

  90. 90.

    , & Ontogeny and adolescent alcohol exposure in Wistar rats: open field conflict, light/dark box and forced swim test. Pharmacol. Biochem. Behav. 122, 279–285 (2014).

  91. 91.

    , , , & Periadolescent ethanol exposure reduces adult forebrain ChAT + IR neurons: correlation with behavioral pathology. Neuroscience 199, 33–45 (2011). This study observed that repeated exposure to alcohol vapour during adolescence disrupts cholinergic neurons in the basal forebrain in adulthood, with these decreases correlating with the amount of disinhibitory behaviour observed in these animals.

  92. 92.

    , , & Periadolescent ethanol vapor exposure persistently reduces measures of hippocampal neurogenesis that are associated with behavioral outcomes in adulthood. Neuroscience 244, 1–15 (2013).

  93. 93.

    , & Effects of pre-test manipulation on elevated plus-maze behavior in adolescent and adult male and female Sprague-Dawley rats. Pharmacol. Biochem. Behav. 92, 413–423 (2009).

  94. 94.

    , & MATSAP: an automated analysis of stretch-attend posture in rodent behavioral experiments. Sci. Rep. 6, 31286 (2016).

  95. 95.

    , , , & Risk-assessment and risk-taking behavior predict potassium-and amphetamine-induced dopamine response in the dorsal striatum of rats. Front. Behav. Neurosci. 8, 236 (2014).

  96. 96.

    et al. Long-term risk preference and suboptimal decision making following adolescent alcohol use. Proc. Natl Acad. Sci. USA 106, 17600–17604 (2009).

  97. 97.

    et al. Risk preference following adolescent alcohol use is associated with corrupted encoding of costs but not rewards by mesolimbic dopamine. Proc. Natl Acad. Sci. USA 108, 5466–5471 (2011).

  98. 98.

    et al. Altered risk-based decision making following adolescent alcohol use results from an imbalance in reinforcement learning in rats. PLoS ONE 7, e37357 (2012).

  99. 99.

    , , , & Adolescent intermittent ethanol exposure is associated with increased risky choice & decrease of dopaminergic & cholinergic neuron markers in adult rats. Int. J. Neuropharmacol. 18, pyu003 (2015).

  100. 100.

    , & Chronic alcohol intake during adolescence, but not adulthood, promotes persistent deficits in risk-based decision making. Alcohol. Clin. Exp. Res. 38, 1622–1629 (2014). This study demonstrates that rats exposed repeatedly to alcohol during adolescence exhibit later increases in risk preference when indexed via an operant probability discounting task.

  101. 101.

    , , & Repeated ethanol exposure during early and late adolescence: double dissociation of effects on waiting and choice impulsivity. Alcohol. Clin. Exp. Res. 38, 2579–2589 (2014).

  102. 102.

    & Adolescence: An Anthropological Inquiry. 1st edn (Free Press, New York, 1991).

  103. 103.

    et al. Effects of ethanol exposure on subsequent acquisition and extinction of ethanol self-administration and expression of alcohol-seeking behavior in adult alcohol-preferring (P) rats: I. Periadolescent exposure. Alcohol. Clin. Exp. Res. 26, 1632–1641 (2002).

  104. 104.

    , & Effects of voluntary access to sweetened ethanol during adolescence on intake in adulthood. Alcohol. Clin. Exp. Res. 37, 1048–1055 (2013).

  105. 105.

    , , , & Long-term ethanol self-administration induces ΔFosB in male and female adolescent, but not in adult, Wistar rats. Prog. Neuropsychopharmacol. Biol. Psychiatry 74, 15–30 (2017).

  106. 106.

    , , & Repeated alcohol administration during adolescence causes changes in the mesolimbic dopaminergic and glutamatergic systems and promotes alcohol intake in the adult rat. J. Neurochem. 108, 920–931 (2009). This paper reports increases in ethanol intake in adulthood following intermittent exposure to alcohol during adolescence, along with alterations in dopaminergic and glutamatergic neurotransmitter systems and histone acetylation in the mesolimbic system.

  107. 107.

    et al. Alcohol intoxications during adolescence increase motivation for alcohol in adult rats and induce neuroadaptations in the nucleus accumbens. Neuropharmacology 67, 521–531 (2013).

  108. 108.

    et al. Effects of ethanol exposure on subsequent acquisition and extinction of ethanol self-administration and expression of alcohol-seeking behavior in adult alcohol-preferring (P) rats: II. Adult exposure. Alcohol. Clin. Exp. Res. 26, 1642–1652 (2002).

  109. 109.

    & Effects of adolescent ethanol exposure on ethanol consumption in adult rats. Alcohol 26, 23–30 (2002).

  110. 110.

    , & Time-course of elevated ethanol intake in adolescent relative to adult rats under continuous, voluntary-access conditions. Alcohol. Clin. Exp. Res. 31, 1159–1168 (2007).

  111. 111.

    , & Gender and age at drinking onset affect voluntary alcohol consumption but neither the alcohol deprivation effect nor the response to stress in mice. Alcohol. Clin. Exp. Res. 32, 100–106 (2008).

  112. 112.

    , & Ethanol pre-exposure during adolescence or adulthood increases ethanol intake but ethanol-induced conditioned place preference is enhanced only when pre-exposure occurs in adolescence. Dev. Psychobiol. 56, 36–48 (2014).

  113. 113.

    , , & Alcohol drinking during adolescence increases consumptive responses to alcohol in adulthood in Wistar rats. Alcohol 59, 43–51 (2017).

  114. 114.

    , & Influence of age at drinking onset on the alcohol deprivation effect and stress-induced drinking in female rats. Pharmacol. Biochem. Behav. 86, 32–26 (2007).

  115. 115.

    , , , & Binge-pattern alcohol exposure during puberty induces long-term changes in HPA axis reactivity. PLoS ONE 6, e18350 (2011).

  116. 116.

    et al. Exposure to alcohol during adolescence exerts long-term effects on stress response and the adult brain stress circuits. Neuroscience 339, 64–71 (2016).

  117. 117.

    , , & Alcohol gains access to appetitive learning through adolescent heavy drinking. Behav. Neurosci. 129, 371–379 (2015).

  118. 118.

    , & Alcohol during adolescence selectively alters immediate and long-term behavior and neurochemistry. Alcohol 44, 57–66 (2010).

  119. 119.

    & Age-related effects of alcohol on memory and memory-related brain function in adolescents and adults. Recent Dev. Alcohol 17, 161–176 (2005).

  120. 120.

    Adolescents and alcohol: acute sensitivities, enhanced intake, and later consequences. Neurotoxicol. Teratol. 41, 51–59 (2013).

  121. 121.

    & Adolescent alcohol exposure and persistence of adolescent typical phenotypes into adulthood: a mini-review. Neurosci. Biobehav. Rev. 45, 1–8 (2014). This paper reviews evidence showing that adolescent exposure to alcohol sometimes results in the persistence of adolescent-typical phenotypes into adulthood that are evident behaviourally, electrophysiologically and in terms of adolescent-typical alcohol sensitivities.

  122. 122.

    et al. Chronic-intermittent ethanol exposure during adolescence prevents normal developmental changes in sensitivity to ethanol-induced motor impairments. Alcohol. Clin. Exp. Res. 26, 960–968 (2002).

  123. 123.

    et al. Reinforcing properties and neurochemical response of ethanol within the posterior ventral tegmental area are enhanced in adulthood by periadolescent ethanol consumption. J. Pharmacol. Exp. Ther. 35, 317–326 (2014).

  124. 124.

    & Consequences of repeated ethanol exposure during early or late adolescence on conditioned taste aversion in rats. Dev. Cogn. Neurosci. 16, 174–182 (2015).

  125. 125.

    , , & Binge pattern ethanol exposure in adolescent and adult rats: differential impact on subsequent responsiveness to ethanol. Alcohol. Clin. Exp. Res. 24, 1251–1256 (2000).

  126. 126.

    , , & Chronic ethanol exposure during adolescence alters the behavioral responsiveness to ethanol in adult mice. Behav. Brain Res. 229, 1–9 (2012).

  127. 127.

    , , & Reduced hippocampal volume among adolescents with alcohol use disorders without psychiatric comorbidity. Psychiatry Res. 139, 181–190 (2005).

  128. 128.

    et al. Prefrontal cortex volumes in adolescents with alcohol use disorders: unique gender effects. Alcohol. Clin. Exp. Res. 32, 386–394 (2008).

  129. 129.

    , , , & Recent binge drinking predicts smaller cerebellar volumes in adolescents. Psychiatry Res. 211, 17–23 (2013).

  130. 130.

    et al. Brain volume reductions in adolescent heavy drinkers. Dev. Cogn. Neurosci. 9, 117–125 (2014).

  131. 131.

    , & The effect of alcohol consumption on the adolescent brain: a systematic review of MRI and fMRI studies of alcohol-using youth. Neuroimage Clin. 5, 420–437 (2014).

  132. 132.

    et al. White matter integrity in adolescents with histories of marijuana use and binge drinking. Neurotoxicol. Teratol. 31, 349–355 (2009).

  133. 133.

    et al. Altered white matter integrity in adolescent binge drinkers. Alcohol. Clin. Exp. Res. 33, 1278–1285 (2009).

  134. 134.

    , , , & Associations between fractional anisotropy and problematic alcohol use in juvenile justice-involved adolescents. Am. J. Drug Alcohol Abuse 39, 365–371 (2013).

  135. 135.

    et al. Not lesser but greater fractional anisotropy in adolescents with alcohol use disorders. Neuroimage Clin. 2, 804–809 (2013).

  136. 136.

    , , , & Level of response to alcohol and brain response during visual working memory. J. Stud. Alcohol 65, 692–700 (2004).

  137. 137.

    et al. Blood oxygen level dependent response and spatial working memory in adolescents with alcohol use disorders. Alcohol. Clin. Exp. Res. 28, 1577–1586 (2004).

  138. 138.

    et al. Gender and adolescent alcohol use disorders on BOLD (blood oxygen level dependent) response to spatial working memory. Alcohol Alcohol. 40, 194–200 (2005).

  139. 139.

    , , & Adolescent binge-drinking linked to abnormal spatial working memory brain activation: differential gender effects. Alcohol. Clin. Exp. Res. 35, 1831–1841 (2011).

  140. 140.

    et al. Volumetric differences in the anterior cingulate cortex prospectively predict alcohol-related problems in adolescence. Psychopharmacology 231, 1731–1742 (2014).

  141. 141.

    , , & Adolescent drinking and brain morphometry: a co-twin control analysis. Dev. Cogn. Neurosci. 16, 130–138 (2015).

  142. 142.

    et al. Orbitofrontal cortex volume and effortful control as prospective risk factors for substance use disorder in adolescence. Eur. Addict. Res. 23, 37–44 (2017).

  143. 143.

    et al. Neural predictors of alcohol use and psychopathology symptoms in adolescents. Dev. Psyhopathol. 28, 1209–1216 (2016).

  144. 144.

    , , & Gray matter volume abnormalities and externalizing symptoms in subjects at high risk for alcohol dependence. Addict. Biol. 12, 122–132 (2007).

  145. 145.

    et al. Right amygdala volume in adolescent and young adult offspring from families at high risk for developing alcoholism. Biol. Psychiatry 49, 894–905 (2001).

  146. 146.

    et al. Amygdala volume in offspring from multiplex for alcohol dependence families: the moderating influence of childhood environment and 5-HTTLPR. J. Alcohol Drug Depend. (Suppl. 1), 001 (2013).

  147. 147.

    et al. Hippocampal volumes in adolescents with and without a family history of alcoholism. Am. J. Drug Alcohol Abuse 36, 161–167 (2010).

  148. 148.

    Family history density of alcoholism relates to left nucleus accumbens volume in adolescent girls. J. Stud. Alcohol Drugs 76, 47–56 (2015).

  149. 149.

    , , , & Amygdala-orbitofrontal connectivity predicts alcohol use two years later: a longitudinal neuroimaging study on alcohol use in adolescence. Dev. Sci. 20, e12448 (2016).

  150. 150.

    , , & Delay discounting behavior and white matter microstructure abnormalities in youth, with a family history of alcoholism. Alcohol. Clin. Exp. Res. 34, 1590–1602 (2010).

  151. 151.

    et al. Frontoparietal connectivity in substance-naive youth with and without a family history of alcoholism. Brain Res. 1432, 66–73 (2012).

  152. 152.

    , , & Resting state functional connectivity of the nucleus accumbens in youth with a family history of alcoholism. Psychiatry Res. 221, 210–219 (2014).

  153. 153.

    et al. Brain response to working memory over three years of adolescence: influence of initiating heavy drinking. J. Stud. Alcohol Drugs 73, 749–760 (2012).

  154. 154.

    , , & A longitudinal examination of adolescent response inhibition: neural differences before and after the initiation of heavy drinking. Psychopharmacology 230, 663–671 (2013). This paper assessed fMRI during a response inhibition task and found that adolescents who later began to drink heavily showed less activation on no-go (relative to go) trials in frontal, parietal and cerebellar regions, whereas they showed greater activation in these regions during performance of the task after the onset of heavy drinking.

  155. 155.

    et al. An FMRI study of response inhibition in youths with a family history of alcoholism. Ann. NY Acad. Sci. 1021, 391–394 (2004).

  156. 156.

    et al. Striatal activity and reduced white matter increase frontal activity in youths with family histories of alcohol and other substance-use disorders performing a go/no-go task. Brain Behav. 5, e00352 (2015).

  157. 157.

    et al. Adolescents at risk for alcohol abuse demonstrate altered frontal lobe activation during Stroop performance. Alcohol. Clin. Exp. Res. 35, 218–228 (2011).

  158. 158.

    & Risky decision-making: an fMRI study of youth at high risk for alcoholism. Alcohol. Clin. Exp. Res. 36, 604–615 (2012).

  159. 159.

    , , & Atypical parietal lboe activity to subliminal faces in youth with a family history of alcoholism. Am. J. Drug Alcohol Abuse 41, 139–145 (2015).

  160. 160.

    , & Incentive-elicited striatal activation in adolescent children of alcoholics. Addiction 103, 1308–1319 (2008).

  161. 161.

    et al. No differences in ventral striatum responsivity between adolescents with a positive family history of alcoholism and controls. Addict. Biol. 20, 534–545 (2015).

  162. 162.

    et al. Brain development in heavy-drinking adolescents. Am. J. Psychiatry 172, 531–542 (2015).

  163. 163.

    , , & Effects of alcohol use initiation on brain structure in typically developing adolescents. Am. J. Drug Alcohol Abuse 39, 345–355 (2013). This paper reports work showing greater developmental declines in grey matter, attenuated increases in white matter and disruptions in white matter integrity over a 2–3-year period of alcohol use during adolescence among a population of youths whose brains did not differ at baseline from those who did not initiate use.

  164. 164.

    , , & Longitudinal changes in white matter integrity among adolescent substance users. Alcohol. Clin. Exp. Res. 37, E181–E189 (2013).

  165. 165.

    et al. The National Consortium on Alcohol and Neuro-Development in Adolescence (NCANDA): a multisite study of adolescent development and substance use. J. Stud. Alcohol Drugs 76, 895–908 (2015).

  166. 166.

    , , & Diffusion tensor imaging reveals adolescent binge ethanol-induced brain structural integrity alterations in adult rats that correlate with behavioral dysfunction. Addict. Biol. 21, 939–953 (2016).

  167. 167.

    , & Neuroimmune activation and myelin changes in adolescent rats exposed to high-dose alcohol and associated cognitive dysfunction: a review with reference to human adolescent drinking. Alcohol Alcohol. 49, 187–192 (2014).

  168. 168.

    , , , & Alcohol binge drinking during adolescence or dependence during adulthood reduces prefrontal myelin in male rats. J. Neurosci. 34, 14777–14782 (2014).

  169. 169.

    et al. TLR4 elimination prevents synaptic and myelin alterations and long-term cognitive dysfunctions in adolescent mice with intermittent ethanol treatment. Brain Behav. Immun. 45, 233–244 (2015).

  170. 170.

    , , , & Intermittent ethanol during adolescence leads to lasting behavioral changes in adulthood and alters gene expression and histone methylation in the PFC. Front. Mol. Neurosci. 10, 307 (2017).

  171. 171.

    , & Brain structure in adolescents and young adults with alcohol problems: systematic review of imaging studies. Alcohol. Alcohol 48, 433–444 (2013).

  172. 172.

    & The burden of binge and heavy drinking on the brain: effects on adolescent and young adult neural structure and function. Front. Psychol. 8, 1111 (2017).

  173. 173.

    et al. Adolescent alcohol exposure decreases frontostriatal resting-state functional connectivity in adulthood. Addict. Biol. (2017). This seminal study examined resting-state MRI in adult rats and observed decreases in connectivity within the PFC and between the PFC and mesolimbic brain regions following repeated alcohol exposure during adolescence.

  174. 174.

    , , & Periadolescent alcohol exposure has lasting effects on adult neurophysiological function in rats. Brain Res. Dev. Brain Res. 128, 63–72 (2001).

  175. 175.

    & Adolescent ethanol exposure: does it produce long-lasting electrophysiological effects? Alcohol 44, 27–37 (2010).

  176. 176.

    et al. P3 components and adolescent binge drinking in Southwest California Indians. Neurotoxicol Teratol 29, 153–163 (2007).

  177. 177.

    , , & Effects of adolescent ethanol exposure on sleep in adult rats. Alcohol 42, 631–639 (2008).

  178. 178.

    , , & The sleep of abstinent pure primary alcoholic patients: natural course and relationship to relapse. Alcohol. Clin. Exp. Res. 22, 1796–1802 (1998).

  179. 179.

    et al. Blunted ventral striatal responses to anticipated rewards foreshadow problematic drug use in novelty-seeking adolescents. Nat. Commun. 8, 14140 (2017).

  180. 180.

    , , & Reversal of alcohol-induced dysregulation in dopamine network dynamics may rescue maladaptive decision-making. J. Neurosci. 36, 3698–3708 (2016). This paper provides evidence to support the suggestion that the increase in risky decision-making after adolescent alcohol exposure is associated with decreases in tonic DA tone, which serve to increase phasic DA responses to rewarding and risky stimuli, driving risky-choice behaviour.

  181. 181.

    , , , & Adolescent alcohol exposure amplifies the incentive value of reward-predictive cues through potentiation of phasic dopamine signaling. Neuropsychopharmacology 40, 2873–2885 (2015).

  182. 182.

    , & Chronic ethanol exposure during adolescence increases basal dopamine in the nucleus accumbens septi during adulthood. Alcohol. Clin. Exp. Res. 31, 895–900 (2007).

  183. 183.

    , & Repeated ethanol exposure during adolescence alters the developmental trajectory of dopaminergic output from the nucleus accumbens septi. Int. J. Dev. Neurosci. 27, 805–815 (2009).

  184. 184.

    , , , & Long-lasting alterations of the mesolimbic dopamine system after periadolescent ethanol drinking by alcohol-preferring rats. Alcohol. Clin. Exp. Res. 28, 702–711 (2004).

  185. 185.

    et al. Binge-like alcohol exposure during adolescence disrupts dopaminergic neurotransmission in the adult prelimbic cortex. Neuropsychopharmacology 42, 1024–1036 (2017). This article shows that adolescent alcohol exposure disrupts DA and GABAergic transmission in the medial PFC, altering development of this brain region, which is critical for behavioural control and decision-making.

  186. 186.

    et al. Voluntary adolescent drinking enhances excitation by low levels of alcohol in a subset of dopaminergic neurons in the ventral tegmental area. Neuropharmacology 110, 386–395 (2016).

  187. 187.

    et al. Reduced dopamine release in the nucleus accumbens core of adult rats following adolescent binge alcohol exposure: age and dose-dependent analysis. Psychopharmacology 232, 777–784 (2015).

  188. 188.

    & Adolescent intermittent ethanol exposure enhances ethanol activation of the nucleus accumbens while blunting the prefrontal cortex responses in adult rat. Neuroscience 293, 92–108 (2015).

  189. 189.

    et al. Adolescent intermittent alcohol exposure: deficits in object recognition memory and forebrain cholinergic markers. PLoS ONE 10, e0140042 (2015).

  190. 190.

    & Adolescent binge ethanol exposure alters specific forebrain cholinergic cell populations and leads to selective functional deficits in the prefrontal cortex. Neuroscience 361, 129–143 (2017).

  191. 191.

    & Chronic binge-like alcohol consumption in adolescence causes depression-like symptoms possibly mediated by the effects of BDNF on neurogenesis. Neuroscience 254, 324–334 (2013).

  192. 192.

    , , & Persistent loss of hippocampal neurogenesis and increased cell death following adolescent, but not adult, chronic ethanol exposure. Dev. Neurosci. 36, 297–305 (2014). This paper presents evidence that repeated exposure to alcohol during adolescence (but not after equivalent exposure in adulthood) exerts long-lasting decreases in neurogenesis that are evident in adulthood well after termination of the chronic exposure.

  193. 193.

    & Persistent decreases in adult subventricular and hippocampal neurogenesis following adolescent intermittent ethanol exposure. Front. Behav. Neurosci. 11, 151 (2017).

  194. 194.

    , , & Alcohol inhibition of neurogenesis: a mechanism of hippocampal neurodegeneration in an adolescent alcohol abuse model. Hippocampus 20, 596–607 (2010).

  195. 195.

    , & Cholinergic influences on cortical development and adult neurogenesis. Behav. Brain Res. 221, 379–388 (2011).

  196. 196.

    et al. Ethanol during adolescence decreased the BDNF levels in the hippocampus in adult male Wistar rats, but did not alter aggressive and anxiety-like behaviors. Trends Psychiatry Psychother. 37, 143–151 (2015).

  197. 197.

    , & Chronic drinking during adolescence predisposes the adult rat for continued heavy drinking: neurotrophin and behavioral adaptation alter long-term, continuous ethanol exposure. PLoS ONE 11, e0149987 (2016).

  198. 198.

    & Addiction, adolescence, and innate immune gene induction. Front. Psychiatry 2, 19 (2011).

  199. 199.

    et al. Toll-like receptor signaling and stages of addiction. Psychopharmacology 234, 1483–1498 (2017).

  200. 200.

    & Binge ethanol exposure during adolescence leads to a persistent loss of neurogenesis in the dorsal and ventral hippocampus that is associated with impaired adult cognitive functioning. Front. Neurosci. 9, 35 (2015).

  201. 201.

    , , , & Intermittent ethanol exposure induces inflammatory brain damage and causes long-term behavioral alterations in adolescent rats. Eur. J. Neurosci. 25, 541–550 (2007).

  202. 202.

    , , , & Involvement of TLR4 in the long-term epigenetic changes, rewarding and anxiety effects induced by intermittent ethanol treatment in adolescence. Brain Behav. Immun. 53, 159–171 (2016). This study provides evidence that repeated exposure to alcohol during adolescence induces neuroimmune activation that likely contributes to the functional consequences of alcohol exposure given that disruption of innate immune receptors protects against exposure-related behavioural and neural consequences.

  203. 203.

    , , & Age and dose-dependent effects of ethanol on the induction of hippocampal long-term potentiation. Alcohol 19, 107–111 (1999).

  204. 204.

    et al. Adolescent intermittent alcohol exposure: persistence of structural and functional hippocampalabnormalities into adulthood. Alcohol. Clin. Exp. Res. 39, 989–997 (2015).

  205. 205.

    et al. Binge-pattern ethanol exposure during adolescence, but not adulthood, causes persistent changes in GABA(a) receptor-mediated tonic inhibition in dentate granule cells. Alcohol. Clin. Exp. Res. 37, 1154–1160 (2013).

  206. 206.

    , , , & In the rat, chronic intermittent ethanol exposure during adolescence alters the ethanol sensitivity of tonic inhibition in adulthood. Alcohol. Clin. Exp. Res. 36, 279–285 (2012).

  207. 207.

    Altered EEG responses to ethanol in adult rats exposed to ethanol during adolescence. Alcohol. Clin. Exp. Res. 26, 246–254 (2002).

  208. 208.

    , & Event-related potential responses to the acute and chronic effects of alcohol in adolescent and adult Wistar rats. Alcohol. Clin. Exp. Res. 38, 749–759 (2014).

  209. 209.

    et al. Chronic Ethanol during adolescence impacts corticolimbic dendritic spines and behavior. Alcohol. Clin. Exp. Res. 41, 1298–1308 (2017).

  210. 210.

    , , & Adolescent alcohol exposure: burden of epigenetic reprogramming, synaptic remodeling, and adult psychopathology. Front. Neurosci. 10, 222 (2016).

  211. 211.

    How to improve the health of American adolescents. Perspect. Psychol. Sci. 10, 711–715 (2015).

  212. 212.

    , , & New neurons in adult brain: distribution, molecular mechanisms and therapies. Biochem. Pharmacol. 141, 4–22 (2017).

  213. 213.

    , , & Use it or lose it: how neurogenesis keeps the brain fit for learning. Behav. Brain Res. 227, 450–458 (2012).

Download references


Preparation of this review was supported by the National Institute on Alcohol Abuse and Alcoholism of the US National Institutes of Health (NIH) under award numbers U01 AA019972 and P50 AA017823. The author thanks A. MacDonald for aiding in the preparation of the reference section, including the reference numbering. The content is solely the responsibility of the author and does not necessarily represent the official views of the NIH.

Author information


  1. Developmental Exposure Alcohol Research Center (DEARC) and Behavioural Neuroscience Program, Department of Psychology, Binghamton University, Binghamton, NY, USA.

    • Linda P. Spear


  1. Search for Linda P. Spear in:

Competing interests

The author declares no competing financial interests.

Corresponding author

Correspondence to Linda P. Spear.


Binge drinking

As defined by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), a pattern of alcohol use that results in blood alcohol concentrations in the range of 0.08 g/dl or greater; typically, alcohol concentrations in this range are achieved by consumption of five or more or four or more drinks within a 2 hour period in males and females, respectively.

Prospective longitudinal studies

Studies that track individuals over time, ideally starting before the emergence of the target measure (for example, in this context, before the initiation of alcohol use or problematic alcohol use).

Set-shifting task

A task in which animals are first taught one rule about the stimulus that predicts a rewarded operant response. There is then a rule shift, and the animals must learn to ignore the initial rule and instead use another stimulus to determine which response will be rewarded.


Learning not to respond when a reinforcer is no longer received.

Elevated plus maze

A test of anxiety that uses a four-armed, cross-shaped apparatus that is well elevated from the floor. Two of the arms are surrounded by high walls (the 'closed arms') whereas the other two arms do not contain walls (the 'open arms'). Anxiety-like behaviour in this test is indexed by animals spending less time and exhibiting fewer entries into the open arms than typically seen in control animals.


A lack of restraint, often associated with increases in impulsivity or risk-taking.

Probability discounting

In an operant probability discounting task, animals are given a choice between a 'safe' lever associated with a small but consistent reward versus a 'risky' lever associated with a reward that is greater but less probable. In such tasks, increased risk-taking is indexed by animals persisting in choosing the risky lever even when the probability of receiving the higher reward is low.

Diffusion tensor imaging

Type of MRI that examines the diffusion of water molecules (which move more rapidly along, rather than across, myelinated axon pathways) to assess the functional integrity of white matter fibre bundles and to index their neuropathology.


A sensory relay area in the brainstem that helps regulate arousal, sleep and autonomic processes.

Dendritic spines

Protuberances on neuronal dendrites that are specialized for receiving synaptic inputs.

About this article

Publication history



Further reading