Table_1_Hyper-Activation of mPFC Underlies Specific Traumatic Stress-Induced Sleep–Wake EEG Disturbances.XLSX (52.79 kB)

Table_1_Hyper-Activation of mPFC Underlies Specific Traumatic Stress-Induced Sleep–Wake EEG Disturbances.XLSX

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posted on 18.08.2020, 07:28 by Tingting Lou, Jing Ma, Zhiqiang Wang, Yuka Terakoshi, Chia-Ying Lee, Greg Asher, Liqin Cao, Zhiyu Chen, Katsuyasu Sakurai, Qinghua Liu

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.

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