Researchers at the University of Oxford in the UK have discovered the molecular switch in the brain that sends us to sleep.
Although the researchers worked on fruit flies for their study, they believe a similar mechanism exists in human brains.
The discovery took place in the laboratory of senior author Prof. Gero Miesenböck at Oxford's Centre for Neural Circuits and Behaviour (CNCB).
Two mechanisms regulate our sleep: one takes into account the external environment, and the other monitors the internal environment.The mechanism that links to the external environment is the body clock, which attunes humans and other animals to the 24-hour day-night cycle.
Researchers studied the internal homeostat that monitors sleep deficit
Researchers have discovered that a molecular switch in the brain that tells us when it is time to sleep.
This new study investigates a "homeostat" mechanism that is attuned to the internal environment and monitors what is happening in the brain. This keeps track of waking hours and tells us when it is time to sleep and reset. It is as though sleep deficit builds up, reaches a point that turns the switch on, and we then start to nod off.
Prof. Miesenböck says:
"What makes us go to sleep at night is probably a combination of the two mechanisms. The body clock says it's the right time, and the sleep switch has built up pressure during a long waking day."
He and his colleagues found the switch works by controlling a handful of sleep-promoting neurons that are active when we are tired and need to sleep, and quieten down when we are fully rested.
One of the lead authors, Dr. Jeffrey Donlea - who specializes in testing new scientific ideas in flies at the CNCB - explains that although they made this new discovery in flies:
"There is a similar group of neurons in a region of the human brain. These neurons are also electrically active during sleep and, like the flies' cells, are the targets of general anesthetics that put us to sleep. It's therefore likely that a molecular mechanism similar to the one we have discovered in flies also operates in humans."
The researchers worked with mutant flies to find the critical part of the sleep switch. They discovered that when certain genes were silenced, the mutant flies could not catch up on lost sleep after they were kept awake all night.
Mutant flies helped researchers discover key mechanism in the sleep homeostat
Prof. Miesenböck likens the sleep homeostat to the thermostat that controls central heating in the home:
"A thermostat measures temperature and switches on the heating if it's too cold. The sleep homeostat measures how long a fly has been awake and switches on a small group of specialized cells in the brain if necessary. It's the electrical output of these nerve cells that puts the fly to sleep."
The researchers found a key molecular component was disabled in the electrical circuit of the mutant flies that kept the sleep-inducing neurons permanently switched off.
The study is important because it may help identify new targets to improve treatments for sleep disorders like insomnia.
However, as the researchers point out, there is still a way to go before any solutions can move from the lab into the clinic.
They also hope that exploring this mechanism and its role further could help answer the big question: "What is the purpose of sleep?"
As a next step, the researchers plan to investigate what internal signal triggers the switch in the first place. They also want to answer questions such as, "What are the sleep-promoting cells monitoring while we are awake?"
Research at the CNBC is funded by the Wellcome Trust and the Gatsby Charitable Foundation, while additional funds from the UK Medical Research Council, the US National Institutes of Health and the Human Frontier Science Program helped finance this particular study, which is published in the journal Neuron.
Medical News Today recently reported on a study suggesting that a good night's sleep may be essential to brain health. Swedish researchers found that depriving healthy young men of a night's sleep increased blood concentrations of brain molecules to levels seen in brain damage.