Lack of sleep has become a common phenomenon in modern life. The study found that people with chronic sleep deprivation may suffer from various diseases caused by lack of sleep, such as decreased thinking ability, impaired alertness and judgment, immune dysfunction, and loss of balance. Let our physical and mental health be violated.
Sleep itself is thought to be a conservative behavior from vertebrates to invertebrates, including flies and nematodes. From the study of existing, it is known that the noradrenergic in the central nervous system regulates sleep. Most receptor subtypes have been screened for validation by studying the network of norepinephrine-regulating neurons. Previous studies have found that βARs in the brain mediate norepinephrine (NE) affecting wakefulness and rapid eye movement (REM) sleep. Clinically, β receptor blockers are widely used and can cause difficulty in falling asleep and keeping sleep, possibly due to reduced production and release of melatonin. In order to find control genes at the molecular level, scientists have screened for potential genes regulating animal sleep homeostasis through large-scale mutagenesis in animal models.
The First Short Sleep Gene: The Discovery of DEC2
As early as 2009, Dr. Ying-Hui Fu, a professor of neuroscience at the University of California, San Francisco, and his team discovered a mutation called DEC2 from a pair of “short sleep” mothers and daughters. It is because of this mutation that they only sleeps for 6 hours a night without significant adverse effects. This is much less than the traditional 7-hour adult sleep time. Further studies have found that DEC2-encoded proteins can reduce the body’s alertness at night by binding and inhibiting MyoD1, a gene that can open orexin. Before dawn, DEC2 levels are lowered, causing MyoD1 to stimulate the production of orexin, which wakes you up and keeps the body alert during the day. Mutations in humans with reduced sleep time diminished the ability of DEC2 to control MyoD1, resulting in excessive orexin production, causing these people to wake up longer. The function of DEC2 may be to ensure that the orexin is expressed at the correct level at the right time every day. Therefore, it is a controller that ensures that the level of the orexin is consistent with the circadian clock.
New Short Sleep Gene: Adrb1 Gene
After further exploration, the researchers found in a family of three generations of genetically “natural short sleep” that no one carried the DEC2 mutation. So what other genes are affecting “natural short sleep”? The researchers used gene sequencing and genetic linkage analysis to determine the exact chromosomal location of the mutation associated with a particular trait to sort out the family’s genome. The study found that a gene mutation called ADRB1, like the DEC2 mutation, is closely related to natural short-term sleep. Since then, the second “natural short sleep gene” has been found! How does this new genetic mutation work for short sleep?
In a batch of genetically engineered mice containing the same ADRB1 mutation as humans, the researchers found that β1AR is expressed at high levels in the dorsal pons (DP). Neuronal activity measured by calcium imaging in this region demonstrates that ADRB1 and neurons in DP are active in wake and REM sleep. Manipulating the activity of these ADRB1 and neurons changes the sleep/wake pattern. Among them, the ADRB1 gene is responsible for encoding the adrenergic beta receptor. In mutational mouse, mutantion results in decreased receptor stability and functional effects. The human mutation was designed into mice, and the mice were reduced in sleep for 55 minutes and immediately awake after light stimulation.