Lack of sleep linked to increased risk of disease and mental health problems

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A group of scientists has identified the mechanism through which stress disrupts the timing of brain cell activity during sleep stages, leading to interrupted sleep and a lack of proper rest, as reported by the “New Atlas,” citing findings from the “Current Biology” journal.

In a mouse model study investigating the physiological impact of stress on sleep, researchers from the University of Pennsylvania focused on the preoptic area (POA) of the hypothalamus. They observed that VGLUT2 neurons, which are more active during wakefulness and less active during sleep, become excessively active during non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep.

Non-rapid eye movement sleep comprises three stages within the 90-minute sleep cycle, with the rapid eye movement stage constituting the fourth. Each stage involves coordinated brain and body functions crucial for health and memory. Stress can induce abnormal firing of VGLUT2 during NREM phases, causing “microexcitations” that disrupt the normal sleep cycle.

Lead researcher Xinghai Zhong, an assistant professor of neuroscience at the University of Pennsylvania, highlighted the widespread effects of poor sleep on memory, immune function, emotional regulation, and appetite. The disruption extends to an increased risk of various diseases and mental health issues, particularly in individuals with stress-related sleep disorders.

While acknowledging that the newfound insight may not directly address the root cause of stress, researchers believe it opens up significant potential for targeting VGLUT2 regulation to suppress these subtle excitations. This approach is deemed particularly relevant for individuals dealing with sleep disorders, anxiety, and post-traumatic stress disorder (PTSD).

According to Chung, understanding the biological factors influencing brain activity during critical sleep stages and how stress disrupts these processes is crucial. He emphasized the potential for developing treatments to promote more restful sleep, allowing the brain to complete essential processes.

The scientists also found that inhibiting VGLUT2 neurons led to a reduction in subtle arousal during NREM sleep, resulting in longer periods of restorative NREM sleep. Jennifer Smith, the primary researcher, emphasized the promising target provided by glutamatergic neurons in the hypothalamus for developing treatments for stress-related sleep disorders. Suppressing VGLUT2 activity could potentially be groundbreaking for individuals experiencing sleep disturbances related to conditions such as insomnia or PTSD.

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