Schepis Ty S, Adinoff Bryon, Rao Uma
Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA.
Am J Addict. 2008 Jan-Feb;17(1):6-23. doi: 10.1080/10550490701756146.
The purpose of this review is to summarize the neurobiological factors involved in the etiology of adolescent addiction and present evidence implicating various mechanisms in its development. Adolescents are at heightened risk for experimentation with substances, and early experimentation is associated with higher rates of SUD in adulthood. Both normative (e.g., immature frontal-limbic connections, immature frontal lobe development) and non-normative (e.g., lowered serotonergic function, abnormal hypothalamic-pituitary-adrenal axis function) neurobiological developmental factors can predispose adolescents to a heightened risk for SUD. In addition, a normative imbalance in the adolescent neurobiological motivational system may be caused by the relative underdevelopment of suppressive mechanisms when compared to stimulatory systems. These neurobiological liabilities may correspond to neurobehavioral impairments in decision-making, affiliation with deviant peers and externalizing behavior; these and other cognitive and behavioral traits converge with neurobiological factors to increase SUD risk. The progression to SUD acts as an amplifying feedback loop, where the development of SUD results in reciprocal impairments in neurobehavioral and neurobiological processes. A clearer understanding of adolescent neurobiology is a necessary step in the development of prevention and treatment interventions for adolescent SUD.
本综述的目的是总结青少年成瘾病因中涉及的神经生物学因素，并呈现表明其发展过程中各种机制的证据。青少年进行物质尝试的风险更高，早期尝试与成年期物质使用障碍（SUD）的高发生率相关。规范性（如额叶 - 边缘系统连接不成熟、额叶发育不成熟）和非规范性（如血清素功能降低、下丘脑 - 垂体 - 肾上腺轴功能异常）神经生物学发育因素均可使青少年易患SUD的风险增加。此外，与刺激系统相比，抑制机制相对发育不足可能导致青少年神经生物学动机系统出现规范性失衡。这些神经生物学缺陷可能与决策方面的神经行为障碍、与不良同伴的交往及外化行为相对应；这些以及其他认知和行为特征与神经生物学因素共同作用，增加了SUD风险。发展为SUD会形成一个放大的反馈回路，其中SUD的发展会导致神经行为和神经生物学过程的相互损害。更清楚地了解青少年神经生物学是制定青少年SUD预防和治疗干预措施的必要步骤。
