New studies have shed light on the impact of stress on sleep by revealing that neurons in the preoptic hypothalamus, a region of the brain responsible for regulating sleep and body temperature, are activated rhythmically during non-rapid eye movement (NREM) sleep. Stress can cause these brain cells to activate out of sync, leading to microarousals that disrupt sleep cycles and reduce the duration of sleep episodes, according to a study by researchers from the Perelman School of Medicine at the University of Pennsylvania, which was published in Current Biology.
Even while our bodies rest during sleep, our brains remain highly active during the four distinct stages of sleep. In each 90-minute sleep cycle, there are three stages of NREM sleep and one stage of rapid eye movement (REM) sleep.
During the first two stages of NREM sleep, brain waves, heartbeat, and breathing slow down, and body temperature decreases. The second stage is characterized by unique brain activity known as spindles and K-complexes, which are short bursts of activity responsible for processing external stimuli and consolidating memory.
In the third stage of the NREM sleep cycle, the body releases growth hormone, which is vital for repairing the body, maintaining a healthy immune system, and enhancing memory.
During this phase, brain waves become larger and are referred to as delta waves. REM sleep, which occurs during this phase and is associated with dreaming, is essential for memory formation, emotional processing, and brain development.
A disrupted night of sleep can lead to problems with memory, emotional instability, and a range of other bodily processes. This is particularly pronounced in individuals with sleep disorders related to stress, said senior author Shinjae Chung, Ph.D., an assistant professor of Neuroscience.
Understanding the underlying biology of brain activity during these crucial stages of sleep and how stimuli like stress can disrupt it is vital in developing therapies to enable individuals to have more restful sleep, allowing their brains to complete these essential processes.
The researchers monitored the activity in the preoptic area (POA) of the hypothalamus in mice during their natural sleep and discovered that glutamatergic neurons (VGLUT2) are activated rhythmically during NREM sleep. They also observed that VGLUT2 neurons are most active during wakefulness and less active during NREM and REM sleep.
During microarousals in NREM sleep, VGLUT2 neurons were the only active neurons in the POA, and their signals began to increase prior to each microarousal.
To confirm that active VGLUT2 neurons were responsible for microarousals, the researchers stimulated these neurons in sleeping subjects, resulting in an immediate increase in microarousals and wakefulness.
Furthermore, the researchers exposed subjects to a stressor to demonstrate the connection between stress and increased VGLUT2 neuron activation. This led to an increase in awake time and microarousals, as well as a decrease in overall time spent in REM and NREM sleep.
The researchers also noted heightened VGLUT2 neuron activity during NREM sleep in the stressed subjects. Additionally, when they inhibited VGLUT2 neurons, microarousals during NREM sleep decreased, and the duration of NREM sleep episodes increased.
The presence of glutamatergic neurons in the hypothalamus provides a promising target for developing treatments for sleep disorders related to stress, stated first author Jennifer Smith, a graduate researcher in Chung’s lab.
The ability to minimize interruptions during the critical stages of NREM sleep by suppressing VGLUT2 activity would be groundbreaking for individuals struggling with disrupted sleep due to disorders such as insomnia or post-traumatic stress disorder (PTSD).
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