Stress is known to elicit contrasting patterns of plasticity in the amygdala and hippocampus. While chronic stress leads to neuronal atrophy in the rodent hippocampus, it has the opposite effect in the basolateral amygdala (BLA). Further, even a single episode of acute stress is known to elicit delayed effects in the amygdala. For example, 2 h of immobilisation stress has been shown to cause a delayed increase in dendritic spine density on BLA principal neurons 10 days later in young rats. This is paralleled by higher anxiety-like behaviour at the same delayed time point. This temporal build-up of morphological and behavioural effects 10 days later, in turn, provides a stress-free time window of intervention after exposure to acute stress. Here, we explore this possibility by specifically testing the efficacy of an anxiolytic drug in reversing the delayed effects of acute immobilisation stress. Oral gavage of diazepam 1 h after immobilisation stress prevented the increase in anxiety-like behaviour on the elevated plus-maze 10 days later. The same post-stress intervention also prevented delayed spinogenesis in the BLA 10 days after acute stress. Surprisingly, gavage of only the vehicle also had a protective effect on both the behavioural and synaptic effects of stress 10 days later. Vehicle gavage was found to trigger a significant rise in corticosterone levels that was comparable to that elicited by acute stress. This suggests that a surge in corticosterone levels, caused by the vehicle gavage 1 h after acute stress, was capable of reversing the delayed enhancing effects of stress on anxiety-like behaviour and BLA synaptic connectivity. These findings are consistent with clinical reports on the protective effects of glucocorticoids against the development of symptoms of post-traumatic stress disorder. Taken together, these results reveal strategies, targeted 1 h after stress, which can prevent the delayed effects of a brief exposure to a severe physical stressor.

众所周知，压力会在杏仁核和海马体中引起不同程度的可塑性。虽然慢性应激会导致啮齿类动物海马神经元萎缩，但对基底外侧杏仁核（BLA）具有相反的作用。此外，已知即使是急性应激的单个发作也会引起杏仁核的延迟作用。例如，已显示2小时的固定压力会导致年轻大鼠10天后BLA主要神经元上树突棘密度的延迟增加。与此同时，在相同的延迟时间点出现了更高的焦虑样行为。10天后，这种形态和行为效应的时间累积反过来为暴露于急性应激后的干预提供了无压力的时间窗。这里，我们通过专门测试抗焦虑药在逆转急性固定应激延迟效应中的功效来探索这种可能性。地西epa的口服管饲1小时后10天后，固定压力阻止了高迷宫中焦虑样行为的增加。相同的应激后干预措施还可以防止急性应激后10天BLA发生旋转延迟。出人意料的是，仅用媒介物管饲也可以在10天后对压力的行为和突触影响产生保护作用。发现车辆管饲会引起皮质酮水平的显着升高，这与急性应激引起的水平相当。这表明，急性应激后1 h的车辆管饲引起的皮质酮水平升高，能够逆转应激对焦虑样行为和BLA突触连接性的延迟增强作用。这些发现与关于糖皮质激素对创伤后应激障碍症状发展的保护作用的临床报道一致。综上所述，这些结果揭示了针对压力后1 h的策略，可以防止短暂暴露于严重的物理压力源的延迟效应。