Adolescence is a developmental period when physical and cognitive abilities are optimized, when social skills are consolidated, and when sexuality, adolescent behaviors, and frontal cortical functions mature to adult levels. Adolescents also have unique responses to alcohol compared with adults, being less sensitive to ethanol sedative-motor responses that most likely contribute to binge drinking and blackouts. Population studies find that an early age of drinking onset correlates with increased lifetime risks for the development of alcohol dependence, violence, and injuries. Brain synapses, myelination, and neural circuits mature in adolescence to adult levels in parallel with increased reflection on the consequence of actions and reduced impulsivity and thrill seeking. Alcohol binge drinking could alter human development, but variations in genetics, peer groups, family structure, early life experiences, and the emergence of psychopathology in humans confound studies. As adolescence is common to mammalian species, preclinical models of binge drinking provide insight into the direct impact of alcohol on adolescent development. This review relates human findings to basic science studies, particularly the preclinical studies of the Neurobiology of Adolescent Drinking in Adulthood (NADIA) Consortium. These studies focus on persistent adult changes in neurobiology and behavior following adolescent intermittent ethanol (AIE), a model of underage drinking. NADIA studies and others find that AIE results in the following: increases in adult alcohol drinking, disinhibition, and social anxiety; altered adult synapses, cognition, and sleep; reduced adult neurogenesis, cholinergic, and serotonergic neurons; and increased neuroimmune gene expression and epigenetic modifiers of gene expression. Many of these effects are specific to adolescents and not found in parallel adult studies. AIE can cause a persistence of adolescent-like synaptic physiology, behavior, and sensitivity to alcohol into adulthood. Together, these findings support the hypothesis that adolescent binge drinking leads to long-lasting changes in the adult brain that increase risks of adult psychopathology, particularly for alcohol dependence.

中文翻译：

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青少年酒精暴露持续影响成人神经生物学和行为。


青春期是身体和认知能力最优化、社交技能得到巩固、性欲、青少年行为和额叶皮质功能成熟到成人水平的发育时期。与成年人相比，青少年对酒精也有独特的反应，对乙醇镇静运动反应不太敏感，而乙醇镇静运动反应很可能导致酗酒和昏厥。人口研究发现，饮酒年龄过早与一生中发生酒精依赖、暴力和伤害的风险增加相关。大脑突触、髓鞘形成和神经回路在青春期成熟到成人水平，同时增加对行为后果的反思，减少冲动和寻求刺激。酗酒可能会改变人类的发育，但遗传学、同侪群体、家庭结构、早期生活经历以及人类精神病理学的出现等方面的差异使研究变得混乱。由于青春期对于哺乳动物来说很常见，因此暴饮暴食的临床前模型可以深入了解酒精对青少年发育的直接影响。这篇综述将人类发现与基础科学研究联系起来，特别是成年青少年饮酒神经生物学 (NADIA) 联盟的临床前研究。这些研究重点关注青少年间歇性饮酒（AIE）（一种未成年人饮酒模式）后成人神经生物学和行为的持续变化。 NADIA 和其他研究发现，AIE 会导致以下结果： 成人饮酒量增加、抑制解除和社交焦虑；改变成人突触、认知和睡眠；减少成人神经发生、胆碱能和血清素能神经元；并增加神经免疫基因表达和基因表达的表观遗传修饰剂。其中许多影响是青少年特有的，在平行的成人研究中没有发现。 AIE 会导致青少年时期的突触生理、行为和对酒精的敏感性持续到成年。总之，这些发现支持了这样的假设：青少年酗酒会导致成人大脑发生长期变化，从而增加成人精神病理学的风险，尤其是酒精依赖。