Department of Psychology, University of California, Los Angeles, CA 90095, USA.
J Clin Child Adolesc Psychol. 2012;41(1):53-63. doi: 10.1080/15374416.2012.632351.
Despite consistent evidence that serotonin functioning affects stress reactivity and vulnerability to aggression, research on serotonin gene-stress interactions (G × E) in the development of aggression remains limited. The present study investigated variation in the promoter region of the serotonin transporter gene (5-HTTLPR) as a moderator of the stress-aggression association at the transition to adulthood. Multiple informants and multiple measures were used to assess aggression in a cohort of 381 Australian youth (61% female, 93% Caucasian) interviewed at ages 15 and 20. At age 20, semistructured interviews assessed acute and chronic stressors occurring in the past 12 months. Structural equation modeling analyses revealed a significant main effect of chronic stress, but not 5-HTTLPR or acute stress, on increases in aggression at age 20. Consistent with G × E hypotheses, 5-HTTLPR short allele carriers demonstrated greater increments in aggression following chronic stress relative to long allele homozygotes. The strength of chronic stress G × E did not vary according to sex. Variation at 5-HTTLPR appears to contribute to individual differences in aggressive reactions to chronic stress at the transition to adulthood.
尽管有一致的证据表明血清素功能会影响应激反应性和攻击倾向，但关于血清素基因-应激相互作用（G×E）在攻击行为发展中的研究仍然有限。本研究探讨了在向成年期过渡期间，5-羟色胺转运体基因（5-HTTLPR）启动子区域的变异作为应激-攻击关联的调节因子。在对 381 名澳大利亚青少年（61%为女性，93%为白种人）进行的一项队列研究中，使用多个知情者和多种测量方法在 15 岁和 20 岁时评估攻击行为。在 20 岁时，半结构化访谈评估了过去 12 个月中发生的急性和慢性应激源。结构方程模型分析显示，慢性应激对 20 岁时攻击行为的增加有显著的主要影响，但 5-HTTLPR 或急性应激没有影响。与 G×E 假设一致，5-HTTLPR 短等位基因携带者在慢性应激后表现出更大的攻击行为增加，相对于长等位基因纯合子。慢性应激 G×E 的强度不随性别而变化。5-HTTLPR 的变异似乎有助于个体对成年期过渡期间慢性应激的攻击反应产生差异。
