Recently, the awakening sleep research team of the Army Medical University published a series of research results in Contemporary Biology and Advanced Science, revealing new targets of melatonin to promote sleep and new functions of melatonin to promote the contraction of neuronal body structure during sleep, providing new ideas for the treatment of insomnia and poor sleep quality. Increasing non rapid eye movement sleep time. Melatonin is a humoral regulatory factor released by the pineal gland and plays an important role in sleep regulation. Professor Hu Zhi'an from the Physiology Teaching and Research Department of the Basic Medical College of the Army Medical University introduced that in clinical practice, taking melatonin or melatonin receptor agonists can help improve sleep disorders. However, the neural mechanisms by which melatonin participates in sleep and whether melatonin has other sleep related functions are currently unclear in academia. A research team consisting of Hu Zhi'an, Professor He Chao from the Army Medical University, and Associate Professor Ren Shuancheng discovered early on that the paraventricular nucleus (PVT) plays an important role in regulating wakefulness and sleep processes. This study revealed the mechanism by which melatonin regulates non rapid eye movement sleep by affecting PVT. It was found that melatonin can inhibit the activity of PVT neurons, increase non rapid eye movement sleep time, and thus facilitate sleep. Hu Zhi'an said that PVT can be understood as a switch in the brain that controls wakefulness and sleep. There are many locks on this switch, which are melatonin type 1 and type 2 receptors, and melatonin is the key to these locks. Melatonin can significantly increase non rapid eye movement sleep time and help people sleep deeper by binding to its receptors and turning off the PVT "switch". On the contrary, if the binding between melatonin and its receptors in PVT is blocked, the duration of non rapid eye movement sleep will decrease and the duration of wakefulness will increase. In addition, studies have found that the expression of melatonin receptors is rhythmic, and the number of melatonin receptors changes with the alternation of day and night. Based on the intrinsic characteristics of PVT neurons during the light dark cycle and the expression pattern of melatonin receptors, it suggests that melatonin mainly plays a sleep guiding role. Specifically, when night falls, melatonin begins to secrete and act on PVT neurons, making it easier for the brain to enter a resting state, "said Hu Zhi'an. This also reminds patients with sleep disorders that when using melatonin as an adjuvant therapy for insomnia, it should not be used as a simple sleeping pill. Maintaining a regular schedule is crucial for maintaining good sleep. The theory of sleep neuron homeostasis suggests that during wakefulness, new information is continuously inputted into the brain. In order to adapt to the needs of information transmission, the volume of neurons continues to increase, which is beneficial for establishing synaptic connections between neurons. However, the volume of neurons will not increase infinitely. During sleep, due to the weakened ability to receive external stimuli, neurons undergo morphological structural retraction to better cope with tasks after waking up the next day. The research team further speculated that melatonin may be involved in the morphological and structural retraction of neurons during sleep, based on the phenomenon that melatonin continues to rise after entering sleep and reaches its peak secretion during sleep. Through research, it has been found that melatonin activates its type 3 receptor after entering sleep, reducing the excitability of memory neurons and promoting the retraction of dendritic spine morphology in neurons during sleep Hu Zhi'an introduced that the research team discovered the phenomenon of dendritic spine morphological structure retraction during sleep in olfactory cortex memory neurons. Four hours of sleep can reduce dendritic spine density by 28%, while sleep deprivation can increase dendritic spine density by 78%. During sleep, the level of melatonin in the entorhinal cortex significantly increases, and memory neurons in the entorhinal cortex highly express melatonin type 3 receptors, while melatonin type 1 and type 2 receptors are expressed at lower levels. If melatonin type 3 receptors are inhibited during sleep, it will significantly cause dysfunction in the dendritic spine morphology of memory neurons. Through the above research, the research team found that when wakefulness enters sleep, the secretion level of melatonin increases. Melatonin reaches the PVT through the cerebrospinal fluid pathway and utilizes the melatonin type 1 and type 2 receptors in the PVT to promote sleep. After entering the sleep period, melatonin will be further secreted, promoting the morphological structure of memory neurons to retract through melatonin type 3 receptors. It can be inferred that melatonin secretion and its receptor signaling impairment may become potential pathological factors for sleep and memory disorders in some major neurological diseases. This will help guide the precise development of drugs for treating insomnia and poor sleep quality Hu Zhi'an said that currently, agomelatine, a drug that activates melatonin type 1 and type 2 receptors, has been used clinically to treat insomnia. In the future, if a combination of type 3 receptor agonists can be developed, it is expected to further improve people's sleep quality and enhance memory ability. (New Society)