According to new research, stress induces a sort of sleep in mice that later relieves worry. A subset of GABA)-somatostatin neurons in the ventral tegmental area (VTA) of the brain receives and is activated by this stress input, promoting both REM (rapid-eye movement) and non-REM sleep, and also inhibiting the release of corticotropin-releasing factor (CRF).
Since sleep is similar to other mammals, it is unlikely that the same mechanism is triggered in human brains. Uncovering the pathways involved might lead to the development of artificial methods to induce beneficial effects, potentially helping to alleviate the psychological stress experienced by people who have just been diagnosed with dementia.
Bill Wisden, PhD, of Imperial University, commented: "Our findings confirm that REM sleep helps us deal with stress." We previously only knew about drugs that inhibit it, such as some medications that suppress it. Now, we have discovered a mechanism by which REM sleep is prevented, opening the way for more medication or other interventions that target the right neurons and boost the stress-fighting ability of sleep.
In a paper titled A specific circuit in the midbrain detects stress and induces restorative sleep, Wisden and his colleagues presented their findings and findings in Science.
The authors concluded that stress can induce insomnia and increase stress hormone levels in rodents, as well as by certain kinds of stress, such as social defeat stress. Thus, sleep has been suggested as a means of alleviating the malign effects of stress.
The researchers hypothesized that stress can induce sleep through the ventral tegmental area of the brain. The VTA regulates reward, aversion, goal-directed behaviors, and social interaction.
According to the authors, mice were exposed to a form of psychosocial stress called social defeat stress, which is used as an analogy for human bullying by exposing them to particularly aggressive mice without physical harm. After the encounter, levels of flight or fight hormones in the mice were monitored by the VTA neurons, which detected and responded to stress hormone levels and induced sleep high in both NREM and REM.
The activity of these neurons, as well as NREM and REM sleep, remained constant for roughly five hours of sleep, during which signals were sent to other neurons that regulate stress hormones, blocking them from releasing more. The newly discovered neurons therefore not only detected stress and induced sleep as a result, but also lowered stress hormones.
The animals' anxiety levels were found to be reduced the following day as a result of the sleep they received. This was assessed by measuring how long the mice spent in the light rather than seeking out darkness as they tend to do more when they are anxious.
mice who didn't get their stress-induced sleep spent far more time in the dark, indicating that they were more anxious, and stress hormone levels remained elevated in these mice. After SDS, CORT [corticosterone] concentrations increased in these mice.
After SDS, CORT concentrations remained elevated in mice who were unable to get SDS-induced sleep, either because their VTASst neurons had been ablated or were inhibited, similar to the effects of sleep deprivation following SDS.
The team hopes to discover methods to selectively target the responsible neurons and boost their positive effects via sleep. This approach might be applied to treat persistent stress disorders such as post-traumatic stress disorder (PTSD). People who suffer from PTSD experience less REM sleep, contributing to the theory that REM sleep helps us process difficult emotions and stress.
Dementia diagnoses can also be a source of enormous psychological stress, and the team hopes that their work will help people cope with a new diagnosis. People with dementia also suffer from more emotional disturbances, and boosting REM sleep may also help alleviate this stress.
Marian Joels, PhD, and E. Ronald de Kloet, PhD, at Leiden University, commented on the findings in the same issue of Science that might assist in future interventions in rodents and perhaps even humans after challenging experiences, whether it be cognitive therapy or genetic interference.
Joels and Kloet conclude that social defeat does not always come with a bout of sleep, and that recent studies suggest that social stress induces sleep-like inactivity in mice, but that this individual variation requires further investigation in larger groups of mice. They say that knowing the essential steps in the brain may assist in future interventions, be it cognitive therapy or genetic interference one day.