In a breakthrough that could reshape our understanding of why we sleep, scientists at the University of Oxford have discovered that the brain’s need for sleep may stem from electrical stress in mitochondria — the tiny energy factories inside cells.

Published in the journal Nature, the study offers one of the first physical explanations for the body’s biological urge to sleep, linking it directly to energy imbalances in the brain.

Led by Professor Gero Miesenböck from the Department of Physiology, Anatomy and Genetics, and Dr Raffaele Sarnataro from Oxford’s Centre for Neural Circuits and Behaviour, the research focused on how mitochondria in sleep-regulating neurons respond to shifts in energy usage.

“When mitochondria become overloaded, they begin to leak electrons, producing harmful reactive oxygen species,” explained Dr Sarnataro. “This acts like an internal warning signal, telling the brain it’s time to rest and repair.”

The team studied fruit flies to monitor sleep behavior and manipulated the electron flow in neurons to measure how mitochondrial stress affected sleep. They found that when electron leakage increased, flies were triggered into sleep, suggesting the brain initiates sleep to prevent broader cellular damage.

Crucially, the study identified specialized neurons that function like circuit breakers, monitoring mitochondrial health and activating sleep once a dangerous threshold is reached.

“You don’t want your mitochondria to leak too many electrons,” said Dr Sarnataro. “That leads to the creation of damaging molecules that can harm cells and brain function.”

The implications of this research extend beyond sleep. Scientists say this discovery could offer new insights into aging, neurodegenerative disorders, and metabolic diseases, all of which are associated with mitochondrial function.

As scientists continue to unravel the mechanics of sleep, this new understanding of energy imbalance as a sleep trigger may open doors to novel therapies for insomnia and other sleep-related conditions.