Chronic stress leads to many psychiatric disorders, including social and anxiety disorders that are associated with over-activation of neurons in the basolateral amygdala (BLA). However, not all individuals develop psychiatric diseases, many showing considerable resilience against stress exposure. Whether BLA neuronal activity is involved in regulating an individual’s vulnerability to stress remains elusive. In this study, using a mouse model of chronic social defeat stress (CSDS), we divided the mice into susceptible and resilient subgroups based on their social interaction behavior. Using in vivo fiber photometry and in vitro patch-clamp recording, we showed that CSDS persistently (after 20 days of recovery from stress) increased BLA neuronal activity in all the mice regardless of their susceptible or resilient nature, although impaired social interaction behavior was only observed in susceptible mice. Increased anxiety-like behavior, on the other hand, was evident in both groups. Notably, the CSDS-induced increase of BLA neuronal activity correlated well with the heightened anxiety-like but not the social avoidance behavior in mice. These findings provide new insight to our understanding of the role of neuronal activity in the amygdala in mediating stress-related psychiatric disorders.

慢性压力会导致许多精神疾病，包括与基底外侧杏仁核（BLA）神经元过度激活有关的社交和焦虑障碍。然而，并非所有个体都会患精神疾病，许多人对压力暴露表现出相当大的恢复能力。BLA 神经元活动是否参与调节个体对压力的脆弱性仍然难以捉摸。在这项研究中，我们使用慢性社交失败应激（CSDS）小鼠模型，根据小鼠的社交互动行为将其分为易感亚组和弹​​性亚组。使用体内光纤光度测定和体外膜片钳记录，我们发现 CSDS 持续（从应激中恢复 20 天后）增加所有小鼠的 BLA 神经元活性，无论其易感性或恢复性如何，尽管社交互动行为受损只是在易感小鼠中观察到。另一方面，两组中焦虑样行为的增加都很明显。值得注意的是，CSDS 诱导的 BLA 神经元活动增加与小鼠的焦虑样增强密切相关，但与社交回避行为无关。这些发现为我们理解杏仁核神经元活动在调节压力相关精神疾病中的作用提供了新的见解。