We all know that stress can rob you of a good night’s sleep, but it’s more than just racing thoughts behind it. For the first time, scientists have identified how stress fires up brain cells at the wrong time during sleep stages, causing interrupted slumber and poor quality of rest.
Investigating the physiological impact of stress on sleep in a mouse model, University of Pennsylvania (UPenn) scientists monitored activity in the preoptic area (POA) of the hypothalamus during natural sleep. They found that glutamatergic neurons (VGLUT2), are most active during wakefulness and less so in non-rapid eye movement sleep (NREM) and rapid eye movement (REM) sleep.
NREM sleep makes up three stages of the 90-minute sleep cycle, with REM being the fourth. Each stage features a cache of coordinated brain and body functions that are key to health and memory.
Stress, however, caused VGLUT2 to fire in NREM stages, when it’s usually subdued, causing “microarousals” that disturbed the regular cycle. When the scientists stimulated the neuron, there was an increase in these microarousals.
While poor sleep impacts memory, immune function, emotional regulation and appetite, it’s also been increasingly linked to heightened risk of disease and mental health issues.
“When you have a bad night of sleep, you notice that your memory isn’t as good as it normally is, or your emotions are all over the place – but a bad night of sleep interrupts so many other processes throughout your body,” said senior author Shinjae Chung, assistant professor of neuroscience at UPenn. “This is even more heightened in individuals with stress-related sleep disorders.”
This discovery may not solve the root cause of the issue – the stress – but the researchers see huge potential in the ability to target VGLUT2 regulation in order to suppress these microarousals.
This could be of particular importance for people with sleep disorders or other conditions such as anxiety and post-traumatic stress disorder (PTSD).
“It’s crucial to understand the biology driving the brain activity in these crucial stages of sleep, and how stimuli like stress can disrupt it, so that we might someday develop therapies to help individuals have more restful sleep that allows their brain to complete these important processes,” Chung added.
The researchers found that when they inhibited VGLUT2 neurons, microarousals during NREM sleep also lessened. Periods of restorative NREM sleep also became longer.
“The glutamatergic neurons in the hypothalamus give us a promising target for developing treatments for stress-related sleep disorders,” said first author, Jennifer Smith, a graduate researcher at UPenn. “Being able to reduce interruptions during the important stages of non-REM sleep by suppressing VGLUT2 activity would be groundbreaking for individuals struggling with disrupted sleep from disorders like insomnia or PTSD.”
The study was published in the journal Current Biology.
Source: University of Pennsylvania
