The study found that glutamate-energy neurons play an important role in sleep stabilization regulation.

On 4 September, the journal Science published a research paper entitled "Regulation of sleep homeostasis mediator adenosine by basal forebrain glutamatergic neurons."
The study was conducted by Xu Min, a researcher at the Center for Brain Science and Intelligent Technology Excellence and Innovation of the Chinese Academy of Sciences (Institute of Neuroscience), the Shanghai Brain Science and Brain Research Center, the National Key Laboratory for Neuroscience, and Li Wei, a researcher at peking university's School of Life Sciences, Peking University-Tsinghua Life Sciences Joint Center, and McGovern Brain Science Research Institute, Peking University. The Dragon Research Group, using a new genetically encoded adenosine probe, found that glutamate-energy neurons in the pre-brain region of the substrate play an important role in regulating the accumulation of sleep stress, and further reveal the neural loop mechanism of sleep steady-state regulation, which provides a reference for exploring treatment methods for sleep disorders.
is a common phenomenon in the animal world, with humans spending about a third of their time sleeping, but current research still doesn't know how sleep is regulated.
classical sleep regulation model, sleep regulation is divided into circadian rhythm and sleep stability.
the circadian rhythm controls the time of the day's sleep awakening through the inner biological clock, and sleep stability is mainly regulated by sleep stress, which controls the amount of sleep the body gets.
sleep stress increases as waking hours progress, and as sleep progresses, sleep stress is gradually removed.
sleep-stabilizing system works when sleep is disturbed, such as staying up late and sleeping more "scented" and longer.
Currently, mainstream theory holds that adenosine is involved in the process of sleep stabilization, and its accumulation in a sobriety state leads to the production of "difficulty", while caffeine, the main ingredient of coffee, can promote sobriety by blocking the binding of adenosine to its receptors.
substrate foremost brain is considered an important brain region in which adenosine is involved in the regulation of sleep stability, and studies at the loop level have shown that local neural loops in this region are involved in the regulation of sleep awakening.
, the mechanism by which neuron activity regulates adenosine release is not yet known, limiting the in-depth analysis of the mechanism of sleep awakening regulation.
In order to detect the high spatial-time resolution of extracellular adenosine concentrations in the precminate region of the substrate during the sleep awakening cycle, Li's team developed a new genetically coded adenosine probe that converts changes in extracellular adenosine concentrations into rapid changes in probe fluorescence intensity.
Using the adenosine probe, Xu Min's team found that adenosine concentrations in the pre-brain region of the substrate were higher when awake and lower during non-rapid eye movement sleep, consistent with previous studies that measured adenosine concentration changes using microdialysis.
, however, the mice had shorter periods of rapid eye movement sleep, and traditional microdialysis methods could not accurately measure adenosine concentration during rapid eye movement sleep.
thanks to the probe's high time resolution, Xu Min's team found for the first time that adenosine also had high concentrations during fast eye movement sleep, higher than awake and non-rapid eye movement sleep.
, the study also observed rapid changes in adenosine concentrations during sleep phase transitions, suggesting that they are closely related to neuron activity.
To further explore the relationship between increased adenosine concentration and neuron activity, Xu Min's team explored the correlation and causality between two types of neurons in the pre-brain region of the substrate, acetylcholine energy neurons and glutamate energy neurons, and changes in adenosine concentration.
results showed that calcium activity of these two neurons was highly associated with extracellular adenosine concentration, and that nerve activity was always released ahead of adenosine.
these two neurons can cause different degrees of increase in extra-cytosine concentration, and glutamate energy neuron activation is the main reason for the increase in adenosine concentration.
further, the researchers specificated the destruction of glutamate-energy neurons in the frontal brain region of the substrate, and the results showed that the increase in extracellular adenosine concentration was significantly lower than in the control group mice.
above tests show that the activities of glutamate-energy neurons are involved in regulating the accumulation of extracellular adenosine.
studies have shown that impaired adenosine accumulation in the pre-brain region of the substrate can lead to abnormal sleep steady-state regulation.
Based on the above experimental results, Xu Min's team speculated that the absence of glutamate-energy neurons in the pre-brain region of the substrate may affect sleep stability, and carried out related studies showing that the sleep stress of mice with glutamate energy neurons in the pre-substrate region decreased significantly (a significant increase in wake-up time), and the sleep steady state also changed - the increase in sleep length after sleep deprivation was significantly lower than that of the control group mice, and the rate of sleep stress removal was significantly faster than that of the control group mice.
above experiments show that glutamate-energy neurons in the pre-brain region of the substrate play an important role in regulating the accumulation of sleep stress.
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