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Abstract：
Sleep disturbances have been recognized as a core symptom of post-traumatic stress disorders (PTSD). However, the neural basis of PTSD-related sleep disturbances remains unclear. It has been challenging to establish the causality link between a specific brain region and traumatic stress-induced sleep abnormalities. Here, we found that single prolonged stress (SPS) could induce acute changes in sleep/wake duration as well as short- and long-term electroencephalogram (EEG) alterations in the isogenic mouse model. Moreover, the medial prefrontal cortex (mPFC) showed persistent high number of c-fos expressing neurons, of which more than 95% are excitatory neurons, during and immediately after SPS. Chemogenetic inhibition of the prelimbic region of mPFC during SPS could specifically reverse the SPS-induced acute suppression of delta power (1-4 Hz EEG) of non-rapid-eye-movement sleep (NREMS) as well as most of long-term EEG abnormalities. These findings suggest a causality link between hyper-activation of mPFC neurons and traumatic stress-induced specific sleep-wake EEG disturbances.
摘要：
睡眠障碍已被认为是创伤后应激障碍（PTSD）的核心症状。然而,PTSD相关睡眠障碍的神经基础尚不清楚.建立特定大脑区域与创伤性压力诱发的睡眠异常之间的因果关系一直具有挑战性。这里,我们发现,在等基因小鼠模型中,单次延长应激(SPS)可引起睡眠/觉醒持续时间的急性变化以及短期和长期脑电图(EEG)改变.此外，内侧前额叶皮质（mPFC）显示出持续大量的c-fos表达神经元，其中95%以上是兴奋性神经元，SPS期间和之后。在SPS期间对mPFC的前边缘区域进行化学遗传抑制可以特异性地逆转SPS引起的非快速眼动睡眠（NREMS）的δ功率（1-4HzEEG）的急性抑制以及大多数长期EEG异常。这些发现表明mPFC神经元的过度激活与创伤应激引起的特定睡眠唤醒EEG干扰之间存在因果关系。
