Clinical evidence indicates that stressful experiences during adolescence can increase rates of posttraumatic stress disorder (PTSD) in adulthood, while prospective evidence from animal models shows that stress in adolescence can increase risk or resilience to the effects of subsequent stress exposure. We discuss recent evidence of lasting effects from adolescent stress in clinical and rodent studies and leverage these findings to evaluate putative biological markers of PTSD etiology. To do this, we evaluate effects of stress in adolescence based on duration, interaction with subsequent stressors, and disease-specificity. We focus on biological systems suggested to integrate effects of developmental stress and distinguish PTSD from related disease states, including hypothalamic-pituitary-adrenal (HPA) axis function, inflammatory cytokine profiles, and epigenetic mechanisms. Our synthesis of recent literature highlights extensive variability in the design of rodent studies of adolescent stress, including stress timing, type, and duration. Given that windows of plasticity fluctuate throughout adolescence, these procedural differences pose challenges for integrating findings. We also find that the majority of recent studies find no lasting effects of adolescent stress on glucocorticoids stress responsivity, such that other biological markers of HPA function may be necessary to capture potential lasting effects of adolescent stress on HPA regulated stress response systems. Conversely, the breadth of early evidence for elevated cytokines highlights both the promise of this field and the challenges from incomplete characterization with respect to sex-differences and non-linear maturation during adolescence. Overall, efforts to map cross-species maturational trajectories, enhance replicability in preclinical findings, and characterize longitudinal trajectories following adolescent stress could facilitate the translation of findings from animal models to clinical contexts.

临床证据表明，青春期的压力经历会增加成年后的创伤后应激障碍（PTSD）的发生率，而动物模型的前瞻性证据表明，青春期的压力会增加患病的风险或对后续压力暴露的影响具有弹性。我们讨论了临床和啮齿动物研究中青春期压力持久影响的最新证据，并利用这些发现来评估PTSD病因的假定生物学标记。为此，我们根据持续时间，与后续压力源的相互作用以及疾病特异性评估青春期压力的影响。我们关注于建议整合发育压力影响并将PTSD与相关疾病状态（包括下丘脑-垂体-肾上腺（HPA）轴功能，炎性细胞因子谱和表观遗传机制）区分开的生物系统。我们对最新文献的综述突显了在啮齿动物青少年应激研究设计中的广泛差异，包括应激时机，类型和持续时间。鉴于可塑性窗口在整个青春期都会波动，因此这些程序上的差异为整合研究结果提出了挑战。我们还发现，最近的大多数研究都没有发现青春期应激对糖皮质激素应激反应的持久影响，因此，可能需要HPA功能的其他生物学标记物来捕获青春期应激对HPA调节的应激反应系统的潜在持久影响。相反，细胞因子升高的早期证据的广度既突出了该领域的前景，又突出了青春期性别差异和非线性成熟方面的不完整表征所带来的挑战。总体而言，努力绘制跨物种成熟轨迹的图谱，可增强临床前研究结果的可复制性，