Last updated on December 24th, 2022 at 11:52 am
Humans sleep for a third of their lives, including invertebrates such as flies, worms and even jellyfish. Sleep has been common and essential to all organisms with nervous systems throughout evolution. But have you ever wondered, Why do we sleep? In fact, scientists have been searching for answers for years. According to a new study published Nov. 18 in the journal Molecular Cell, researchers at Bar-Ilan University in Israel have found that the PARP1 protein in the brain acts as an “antenna” that signals the time to sleep and repair DNA damage to the brain , the discovery is one step closer to solving the mystery.
Why do People sleep?
Homeostatic sleep pressure in the body increases when we are awake, and the longer we stay awake, the greater this pressure. Factors such as UV light, neuronal activity, radiation, oxidative stress, and other factors can cause sustained DNA damage in neurons during the waking hours. However, excessive DNA damage in the brain can be dangerous, and sleep can “call on” the DNA repair system.
The characteristics of neural activity during sleep in zebrafish are similar to those of humans, and they are the object of sleep research. Using zebrafish experiments, the researchers determined that the accumulation of DNA damage is the driver of the sleep state. When the accumulation of DNA damage reaches a maximum threshold, the steady-state sleep pressure increases to trigger the urge to sleep, and the fish goes to sleep. Subsequent sleep promotes DNA repair, which reduces DNA damage.
The study also found that at least 6 hours of sleep was required to reduce homeostatic sleep stress and repair DNA damage.
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So, what mechanism in the brain tells us:
Time to sleep? The study found that the PARP1 protein is part of the DNA damage repair system and is one of the first to respond quickly. It marks the location of DNA damage in cells and “recruits” all relevant systems to clear the DNA damage.
Through genetic and pharmacological manipulation, PARP1 overexpression and knockdown (expression downregulation) experiments showed that increasing PARP1 not only promotes sleep, but also increases sleep-dependent repair. Conversely, inhibiting PARP1 blocked signals for DNA damage repair. As a result, the fish didn’t fully realize they were tired, so they didn’t go into sleep mode, leaving DNA damage that wasn’t repaired in time. The same experimental results were also confirmed in mice.
The new discovery describes how sleep’s “chain of events” is explained at the single-cell level. This mechanism could explain the link between sleep disturbances, aging, and neurodegenerative diseases such as Parkinson’s and Alzheimer’s. The researchers believe that future research will be able to expand to more other animals, including from lower invertebrates to humans.