Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected after acute swim stress

We show that traumatic stress experienced by males in early postnatal life impairs memory in their offspring, blocks long-term potentiation (LTP) and favors long-term depression (LTD). These effects are accompanied by suppression of key molecular pathways involved in neuronal plasticity both at rest and after acute stress. Male mice were exposed to chronic traumatic stress in early postnatal life and were later bred to naïve females to produce second-generation offspring. Memory performance was evaluated in the offspring, and synaptic plasticity was examined in the hippocampus and the amygdala, brain areas important for memory formation. The two groups tested were 1: offspring of fathers which were stressed (MSUS - maternal separation unpredictable stress) and 2: offspring of non-stressed fathers (control). Genome-wide gene expression in hippocampus of these two groups was assessed at rest and after acute stress (this study).

本研究证实，雄性个体在早期产后阶段经历的创伤应激会损伤其子代的记忆功能，阻断长时程增强（long-term potentiation, LTP）并促进长时程抑制（long-term depression, LTD）。此类效应同时伴随静息状态与急性应激后神经元可塑性相关关键分子通路的抑制。
本研究将雄性小鼠于早期产后生命周期内暴露于慢性创伤应激环境，随后与未经历应激的雌性小鼠交配，获得第二代子代。研究人员对受试子代的记忆表现进行了评估，并在记忆形成相关的重要脑区——海马体与杏仁核中检测了突触可塑性。
本研究设置两组受试对象：1. 父亲曾接受慢性创伤应激的子代（MSUS，即母婴分离不可预测应激（maternal separation unpredictable stress））；2. 父亲未经历应激的子代（对照组）。本研究还对两组受试对象海马体的全基因组基因表达水平进行了检测，分别在静息状态与急性应激后开展评估。