Why do people sleep?
Scientists give further answers
Humans sleep a third of their lives, including invertebrates such as flies, worms and even jellyfish.
Throughout the evolutionary process, sleep is universal and essential for all organisms with a nervous system.
But have you ever thought about why we should sleep?
In fact, scientists have been searching for answers for years.
According to a new study published in the journal Molecular Cell on November 18, researchers at Bar-Ilan University in Israel found that the PARP1 protein in the brain is like an "antenna" that can send time signals to the brain to sleep and repair DNA damage. , This discovery is one step closer to solving this mystery.
When we are awake, the steady-state sleep pressure in the body will increase. The longer we stay awake, the greater the pressure.
During the waking hours, ultraviolet rays, neuronal activity, radiation, oxidative stress and other factors can cause continuous damage to the DNA in the neurons.
However, excessive DNA damage in the brain can be dangerous, and sleep can "call" the DNA repair system.
Zebrafish's neural activity characteristics during sleep are similar to those of humans, and they are the subject of sleep research.
Through zebrafish experiments, the researchers determined that the accumulation of DNA damage is the driving factor that causes sleep.
When the accumulation of DNA damage reaches the maximum threshold, the steady-state sleep pressure increases to trigger the urge to sleep, and the fish enters a sleep state.
The subsequent sleep promotes DNA repair, thereby reducing DNA damage.
The study also found that it takes at least 6 hours of sleep to reduce steady-state sleep stress and repair DNA damage.
So, what mechanism in the brain tells us: it's time to sleep?
Studies have found that PARP1 protein is part of the DNA damage repair system and is one of the first proteins to respond quickly.
It can mark the location of DNA damage in cells and "recruit" all relevant systems to eliminate DNA damage.
Through genetic and pharmacological manipulation, PARP1 overexpression and knockdown (down-regulation) experiments show that increasing PARP1 can not only promote sleep, but also increase sleep-dependent repair.
Conversely, inhibiting PARP1 will block the signal for DNA damage repair.
As a result, these fish are not fully aware that they are tired, so they will not enter sleep mode, causing DNA damage not to be repaired in time.
The same experimental results have also been verified in mice.
This new discovery describes how to explain the "event chain" of sleep at the single-cell level.
This mechanism may explain the connection between sleep disorders, aging, and neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease.
Researchers believe that future related research will be able to extend to more other animals, including lower invertebrates to humans.