Gupta Kanika, Chattarji Sumantra
National Centre for Biological Sciences, Bangalore, 560065, India.
Neurobiol Stress. 2021 Jan 7;14:100292. doi: 10.1016/j.ynstr.2020.100292. eCollection 2021 May.
There is accumulating evidence that stress triggers specific temporal patterns of morphological plasticity in the amygdala, a brain area that plays a pivotal role in the debilitating emotional symptoms of stress-related psychiatric disorders. Acute immobilization stress is known to cause a delayed increase in the density of dendritic spines on principal neurons in the basolateral amygdala (BLA) of rats. These neuronal changes are also accompanied by a delayed enhancement in anxiety-like behavior. However, these earlier studies used male rats, and the delayed behavioral and synaptic effects of acute stress on the BLA of female rats remain unexplored. Here, using whole-cell recordings in rat brain slices, we find that a single exposure to 2-h immobilization stress leads to an increase, 10 days later, in the frequency of miniature excitatory postsynaptic currents (mEPSCs) recorded from lateral amygdala (LA) principal neurons in male rats. Further, acute stress also causes a reduction in the frequency of miniature inhibitory postsynaptic currents (mIPSCs) in LA neurons 10 days after acute stress. In striking contrast, excitatory and inhibitory synaptic transmission in the LA of female rats does not exhibit any delayed change despite exposure to the same acute stress. Finally, we examined the functional impact of these contrasting synaptic changes at the behavioral level. Male rats exhibit a delayed increase in anxiety-like behavior on the elevated plus-maze 10 days after acute stress. However, the same stress does not lead to a delayed anxiogenic effect in female rats. Together, these results demonstrate that the delayed modulation of the balance of synaptic excitation and inhibition in the amygdala, as well as anxiety-like behavior, differ between males and females. These findings provide a framework, across biological scales, for analyzing how affective symptoms of stress disorders vary between the sexes.
越来越多的证据表明，压力会触发杏仁核中特定的形态可塑性时间模式，杏仁核是一个在与压力相关的精神疾病使人衰弱的情绪症状中起关键作用的脑区。已知急性固定应激会导致大鼠基底外侧杏仁核（BLA）中主要神经元的树突棘密度延迟增加。这些神经元变化还伴随着焦虑样行为的延迟增强。然而，这些早期研究使用的是雄性大鼠，急性应激对雌性大鼠BLA的延迟行为和突触效应仍未得到探索。在这里，我们使用大鼠脑片的全细胞记录发现，单次暴露于2小时的固定应激会在10天后导致雄性大鼠外侧杏仁核（LA）主要神经元记录的微小兴奋性突触后电流（mEPSCs）频率增加。此外，急性应激还会在急性应激10天后导致LA神经元的微小抑制性突触后电流（mIPSCs）频率降低。与之形成鲜明对比的是，尽管暴露于相同的急性应激下，雌性大鼠LA中的兴奋性和抑制性突触传递并未表现出任何延迟变化。最后，我们在行为水平上研究了这些对比性突触变化的功能影响。雄性大鼠在急性应激10天后在高架十字迷宫上表现出焦虑样行为的延迟增加。然而，相同的应激并不会导致雌性大鼠出现延迟的致焦虑效应。总之，这些结果表明，杏仁核中突触兴奋和抑制平衡的延迟调节以及焦虑样行为在雄性和雌性之间存在差异。这些发现提供了一个跨生物尺度的框架，用于分析应激障碍的情感症状在性别之间是如何变化的。
