prevented the unusual high amounts of non-REM sleep, and on the flip side, its chronic activation in un-stressed mice resulted in extra non-REM sleep.
Next, by separately activating habenular neurons that send signals to different regions of the brain, the researchers were able to identify the connection between the habenula and the rostromedial tegmental nucleus as critical. Activating only these neurons mimicked the effects of stress on sleep, while inhibiting them in stressed mice mimicked the effects of bright-light treatment.
Lastly, the researchers showed that light-sensitive neurons in the lateral geniculate nucleus naturally inhibit the habenula-RMT neurons, which explains why bright-light treatment can reduce stress-induced abnormalities in non-REM sleep. Understanding how bright-light treatment works can help devise optimal light treatments and perhaps pharmacological interventions targeting this pathway.
Co-author Chaoran Ren adds,"A circuit mechanism has been identified that explains the effects of bright light treatment on sleep disruptions induced byBright light treatment counteracts stress-induced sleep alterations in mice, via a visual circuit related to the rostromedial tegmental nucleus,
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