Curr Biol: Sleep less and don't get sleepy, an enviable genetic mutation that causes natural short sleep.

Today, every day of work, study and life make us stressed, it can be said that in the adult world, in addition to hair loss, obesity and sleep, everything else is not easy.
But it has to be said that human and human physique can not be generally general, some people sleep eight hours a day is far from enough, and some people only sleep four hours a day is more than enough.
natural short sleep refers to the average life-long sleep time is less than 6.5 hours, and there is no detectable adverse physiological reactions to the sleep habits.
why do these people sleep less and not get sleepy? What gives them this enviable ability to envy hate? On October 15, 2020, at the University of California, , Louis J. Ptá? As co-author of the paper, ek published a research paper in the cell sub-journal Current Biology entitled: Mutations in Metabotropic Glutamate Receptor 1 Contribute to Natural Short Sleep Trait.
study found two different mutations in the same gene that causes natural short sleep, the metabolic glutamate-like lily 1 (GRM1).
More importantly, both people and mice carrying the gene mutation showed short sleep behavior, and brain slices showed that both mutations altered the nerve properties of the brain, increasing excited synhap delivery and leading to short sleep esoterics.
It is well known that for most adults, 7-8 hours of sleep per day is necessary to maintain physical and mental health, but for natural short sleepers (NSSs), 4-6 hours of sleep per day is sufficient and does not have any significant adverse effects on health.
it is indisputable that the mechanism by which sleep is regulated is a very complex process, so in order to understand the mechanisms that lead to this difference between natural short sleepers and normal sleepers, Fu hui and Louis Ptá? The team, led by ek, has been looking for genetic variants that lead to short sleep behavior traits.
In the study, researchers reported mutations at two different locations in two unrelated families of families of natural short sleep (FNSS), which encodes the metabolic glutamate complex mGluRs, a variant that is often present in the cell membrane in the form of a diogenes.
previous studies that found two mutations in the GRM1 gene in two unrelated FNSS families showed that mGluR1/5 was involved in a wide range of physiological processes and was associated with sleep regulation.
, mGluR5 knock-out mice showed severe sleep-awakening steady-state disorders.
, however, despite these related studies, there is no direct evidence of the role of mGluR1 in sleep regulation.
note that glutamate is an excitable neurotransmitter, but in most cases the activation of metabolic glutamate receptors reduces the activity of ionized glutamate receptors.
, if the GRM1 mutation causes a defect in the function of the subject, the excitable synhaplic delivery mediated by glutamate should be increased in neurons that express the gene.
to this, the team first confirmed through a series of in-body experiments that both mutations showed a loss of conductor-mediated signal transductivity, suggesting that the GRM1 mutation could indeed affect the excited synapse delivery of the associated neurons.
mGluR1s were less active in Tango Assays, the team used CRISPR gene editing techniques to model mice with GRM1 mutations and recorded their sleep patterns.
found that the GRM1 mutation can cause changes in sleep duration - GRM1 mutant mice sleep about half an hour shorter a day than normal mice.
GRM1 mutation reduced the total sleep time of the FNSS mouse model in addition to the relevant electrophysiological experiments, the researchers observed an increase in glutamate-mediated excited synhap delivery in the brain slice of the GRM1 mutant mouse model, once again confirming that the GRM1 mutation led to a decrease in the function of the subject.
, both mutations alter the brain's neural properties and increase excited synapse delivery.
In fact, professor Fuhui and others have previously made similar findings - ADRB1, NPSR1 mutants can lead to increased cell excitability, suggesting that short sleep gene mutations can increase the likelihood of waking time by increasing neuron excitability
Grm1 mutation altered the electrophysiological properties of Grm1 plus neurons slightly, and the team compared previously discovered short sleep genes - ADRB1 and NPSR1, both of which reduced sleep time by about an hour in mouse models.
, the short sleep esoteric esotypes caused by the GRM1 mutation are slightly weaker than they were.
this, the authors suggest that other genetic factors may work in synergy with the GRM1 mutation to change the amount of sleep the body needs.
they will reveal this possibility by building models of mice with multiple mutations.
all, the study showed that GRM1 is another short sleep gene, and that people and mice with the mutation will show shorter sleep times.
, the study also highlights the important role of the metabolic glutamate-like subject, mGluRs, in regulating human sleep.
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