Why do people sleep? A new study points to the brain
Experiments on fruit flies suggest tiredness could be caused by damaged
neurons
IT IS HARD to overstate the importance of sleep. Regular hours of rest
offer organisms of all sizes a chance to consolidate memories, repair cells
and boost the health of their immune systems. But the source of the urge to
sleep, known to scientists as sleep pressure (and everyone else as
tiredness), has remained elusive.
Many theories have been put forward. One pins the blame on the
build-up of a brain chemical called adenosine. Another points the finger at
the brain’s need to build synaptic connections. A study published in Nature
on July 16th offers the strongest evidence yet that the urge to sleep is
caused by a build-up of electrons in the mitochondria of certain brain
cells. If true, sleep may have originally emerged as a way of repairing
mitochondria, with its other benefits evolving later.
Mitochondria, which can be found in almost all human and animal
cells, supply energy by stripping electrons from fuel molecules derived
from food. But some electrons leak out of the mitochondria while this takes
place, reacting with oxygen to produce toxic by-products that can damage
the mitochondria, as well as other parts of the cell, if they build up.
The new study suggests that when too much mitochondrial damage is
detected in brain cells known as sleep-control neurons, they trigger sleep.
These neurons act like circuit-breakers, says Gero Miesenböck at Oxford
University, one of the paper’s lead authors, tripping the brain into sleep
before too many electrons build up. Sleep simultaneously restores the
balance of electrons and allows the mitochondrial damage to be repaired.
To reach their conclusions, the scientists conducted a series of
experiments on fruit flies. They started by labelling the sleep-control
neurons in the flies’ brains, known as dorsal fan-shaped body neurons
(dFBNs), with a genetically engineered protein that made them glow green.
They then disrupted the flies’ natural sleep cycles by placing them on a
platform that was kept in constant motion for 12 hours.
When the fluorescent dFBNs were subsequently viewed under a
microscope, the mitochondria within were found to have split apart, a sign
of electron-related damage. After a period of sleep, however, they had
fused back together.
This suggested that mitochondrial damage might drive the urge to
sleep. To determine if the relationship was causal, the scientists then
manipulated the balance of electrons in the mitochondria in several other
ways.
Most telling was an experiment in which the researchers provided
mitochondria in the dFBNs with an alternative power source: namely a
protein that uses light for energy. When the researchers shone a flashlight
on flies that were not sleep-deprived, their mitochondria could supply
energy without needing to use their stash of electrons. This increased the
chance of an electron leak. Within the first hour of exposure to the
flashlight the engineered flies were much more likely to fall asleep than
those in control groups.
Ivana Rosenzweig, a specialist in the neuroscience of sleep at King’s
College London who was not involved in the study, says that the findings
represent a significant conceptual shift. Although electron imbalance in
mitochondria had been suspected to correlate with a lack of sleep, she
believes this study provides evidence that it may be the cause of sleep
pressure. As the way cells are supplied with energy is closely linked to
sleep across many animal species, the authors say it is likely that
electron build-up could cause sleep pressure in humans, too. They further
note that humans with mitochondrial disorders often report a feeling of
sleepiness unrelated to muscle fatigue. Professor Miesenböck hopes that a
better understanding of sleep pressure will help shed light on a range of
sleep disorders and chronic conditions that count fatigue as a symptom. ■
KR IRS 6925
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