ArticleFrontiers in neuroscience2020
Hyper-Activation of mPFC Underlies Specific Traumatic Stress-Induced Sleep-Wake EEG Disturbances.
Article in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Preventing traumatic stress-induced behavioral abnormalities in rats with blue light phototherapy.Translational psychiatry · 2026Article
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- Unlocking NAC's potential ATF4 and m6A dynamics in rescuing cognitive impairments in PTSD.Metabolic brain disease · 2025Article
- The impact of MDQ positivity on quality of life impairment: Does it support the hypothesis of "Dysregulation of Mood, Energy, and Social Rhythms Syndrome" (DYMERS)?Journal of public health research · 2023Article
- Preventing Post-Traumatic Stress Disorder (PTSD) in rats with pulsed 810 nm laser transcranial phototherapy.Translational psychiatry · 2023Article
- Sex differences in chronic pain-induced mental disorders: Mechanisms of cerebral circuitry.Frontiers in molecular neuroscience · 2023Review
- Dopaminergic Neurons in the Ventral Tegmental-Prelimbic Pathway Promote the Emergence of Rats from Sevoflurane Anesthesia.Neuroscience bulletin · 2022Article
- Article
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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