Long Kimberly L P, Muroy Sandra E, Sorooshyari Siamak K, Ko Mee Jung, Jaques Yanabah, Mohan Kishant, Sudmant Peter, Kaufer Daniela
Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, 94720, USA.
Department of Integrative Biology, University of California, Berkeley, Berkeley, CA, 94720, USA.
Neurobiol Stress. 2025 Aug 26;38:100754. doi: 10.1016/j.ynstr.2025.100754. eCollection 2025 Sep.
Traumatic experiences elicit a wide range of cognitive responses in both humans and animals, leading to diverse outcomes such as enhanced performance, cognitive impairment, or the development of mood and anxiety disorders like posttraumatic stress disorder (PTSD). A key challenge in understanding these varied responses is to decipher the underlying biological mechanisms that contribute to individual variability in trauma resilience or susceptibility. The purpose of this study was to elucidate the molecular bases for these differences, focusing on the amygdala and hippocampus-brain regions integral to stress responses. We exposed adult, male rats to an acute, severe stressor and profiled persistent anxiety-like behavior outcomes 7 days later. We investigated the transcriptional signatures in the basolateral amygdala and hippocampal dentate gyrus via bulk RNA sequencing from animals with behavioral outcomes indicative of stress resilience or vulnerability. Our results suggest that the basolateral amygdala and dentate gyrus display distinct transcriptomic changes following acute, severe stress. Furthermore, we identified specific region-dependent genes related to insulin signaling, neural plasticity, and stress responses that correlate with resilient and vulnerable phenotypes. Notably, a larger number of genes separated stress-resilient animals from both control and stress-susceptible animals, underscoring that an active molecular response, particularly in the hippocampus, facilitates protection from the long-term consequences of severe stress. These findings provide novel insight into the mechanisms that engender individual variability in the behavioral responses to stress and offer new targets for the advancement of therapies for stress-induced neuropsychiatric disorders.
创伤性经历会在人类和动物身上引发广泛的认知反应,导致多种结果,如表现增强、认知障碍,或出现创伤后应激障碍(PTSD)等情绪和焦虑障碍。理解这些不同反应的一个关键挑战是破译导致个体在创伤恢复力或易感性方面存在差异的潜在生物学机制。本研究的目的是阐明这些差异的分子基础,重点关注杏仁核和海马体——对应激反应至关重要的脑区。我们让成年雄性大鼠暴露于急性严重应激源下,并在7天后分析持续的焦虑样行为结果。我们通过对行为结果表明具有应激恢复力或易感性的动物进行批量RNA测序,研究了基底外侧杏仁核和海马齿状回中的转录特征。我们的结果表明,基底外侧杏仁核和齿状回在急性严重应激后表现出不同的转录组变化。此外,我们确定了与胰岛素信号传导、神经可塑性和应激反应相关的特定区域依赖性基因,这些基因与恢复力和易感性表型相关。值得注意的是,大量基因将应激恢复力强的动物与对照组和应激易感动物区分开来,这突出表明,尤其是在海马体中的一种活跃分子反应有助于保护机体免受严重应激的长期影响。这些发现为导致个体对应激行为反应存在差异的机制提供了新的见解,并为推进应激诱导的神经精神障碍治疗方法提供了新的靶点。