Summary: Researchers unveiled the neural pathway linking chronic stress to sleep disturbances, shedding light on how bright-light treatment rectifies these issues.
The study, involving mouse models, emphasized the crucial role of the lateral habenula, a brain region sensitive to light signals. When activated, this region influenced non-REM sleep patterns.
Interestingly, bright-light treatment was found to inhibit certain neurons, reducing sleep abnormalities caused by stress.
Chronic stress can increase non-REM sleep, which bright-light treatment can counter.
The lateral habenula, a part of the brain sensitive to light signals, plays a pivotal role in mediating the effects of stress on sleep.
Bright-light treatment works by inhibiting the habenula-RMT neurons, thus reducing stress-induced non-REM sleep abnormalities.
Chronic stress is associated with sleep disturbance. In their new study, Lu Huang and colleagues identify the neural pathway behind this behavior, and at the same time, explain how bright-light treatment is able to counter it.
The research was conducted in mice at Jinan University in China and published September 7th in the open access journal PLOS Biology.
Bright-light treatment is known to improve sleep in those with sleep disorders, but how it works – and whether it works in cases of stress-induced sleep disturbances – was unknown.
The researchers hypothesized that a part of the brain called the lateral habenula is deeply involved in this phenomenon because it both receives light signals from the eyes and can influence other parts of the brain that regulate sleep.
To test this theory and fully characterize the neural pathway, the team performed a series of chemogenetic and optogenetic studies in a mouse model of chronic stress, which also showed irregular sleep. Specifically, chronic stress led to higher-than-normal amounts of non-REM sleep, which could be eliminated with bright-light treatment.
As hypothesized, the lateral habenula influenced the effects of stress on sleep. Its chemogenetic inhibition in stressed mice 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 (RMT) 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 (LGN) 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.
Coauthor Chaoran Ren adds, “A circuit mechanism has been identified that explains the effects of bright light treatment on sleep disruptions induced by chronic stress in mice.”
About this stress and sleep research news
Author: Charlotte Bhaskar Source: PLOS Contact: Charlotte Bhaskar – PLOS Image: The image is credited to Neuroscience News
Bright light treatment counteracts stress-induced sleep alterations in mice, via a visual circuit related to the rostromedial tegmental nucleus
Light in the environment greatly impacts a variety of brain functions, including sleep. Clinical evidence suggests that bright light treatment has a beneficial effect on stress–related diseases.
Although stress can alter sleep patterns, the effect of bright light treatment on stress–induced sleep alterations and the underlying mechanism are poorly understood.
Here, we show that bright light treatment reduces the increase in nonrapid eye movement (NREM) sleep induced by chronic stress through a di–synaptic visual circuit consisting of the thalamic ventral lateral geniculate nucleus and intergeniculate leaflet (vLGN/IGL), lateral habenula (LHb), and rostromedial tegmental nucleus (RMTg).
Specifically, chronic stress causes a marked increase in NREM sleep duration and a complementary decrease in wakefulness time in mice. Specific activation of RMTg–projecting LHb neurons or activation of RMTg neurons receiving direct LHb inputs mimics the effects of chronic stress on sleep patterns, while inhibition of RMTg–projecting LHb neurons or RMTg neurons receiving direct LHb inputs reduces the NREM sleep–promoting effects of chronic stress.
Importantly, we demonstrate that bright light treatment reduces the NREM sleep–promoting effects of chronic stress through the vLGN/IGL–LHb–RMTg pathway.
Together, our results provide a circuit mechanism underlying the effects of bright light treatment on sleep alterations induced by chronic stress.