Good news! I think, I can relate to that. Will we soon have better sleeping pills?
"... Investigating the physiological impact of stress on sleep in a mouse model, ... 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. ..."
From the highlights and abstract:
"Highlights
• POA glutamatergic neurons become activated during microarousals in NREM sleep
• Stress activates POA glutamatergic neurons, leading to fragmented sleep
• Inhibiting POA glutamatergic neurons attenuates stress-induced sleep fragmentation
• Presynaptic inputs in the lateral hypothalamus become activated after stress
Summary
Sleep disturbances are detrimental to our behavioral and emotional well-being. Stressful events disrupt sleep, in particular by inducing brief awakenings (microarousals, MAs), resulting in sleep fragmentation. The preoptic area of the hypothalamus (POA) is crucial for sleep control. However, how POA neurons contribute to the regulation of MAs and thereby impact sleep quality is unknown. Using fiber photometry in mice, we examine the activity of genetically defined POA subpopulations during sleep. We find that POA glutamatergic neurons are rhythmically activated in synchrony with an infraslow rhythm in the spindle band of the electroencephalogram during non-rapid eye movement sleep (NREMs) and are transiently activated during MAs. Optogenetic stimulation of these neurons promotes MAs and wakefulness. Exposure to acute social defeat stress fragments NREMs and significantly increases the number of transients in the calcium activity of POA glutamatergic neurons during NREMs. By reducing MAs, optogenetic inhibition during spontaneous sleep and after stress consolidates NREMs. Monosynaptically restricted rabies tracing reveals that POA glutamatergic neurons are innervated by brain regions regulating stress and sleep. In particular, presynaptic glutamatergic neurons in the lateral hypothalamus become activated after stress, and stimulating their projections to the POA promotes MAs and wakefulness. Our findings uncover a novel circuit mechanism by which POA excitatory neurons regulate sleep quality after stress."
Penn Medicine research shows how stress activates neurons that disrupt sleep Suppressing these neurons may be a promising target for therapies to treat stress-related sleep disorders, like insomnia and PTSD
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