The study, which explored how sedatives work in the brain's neural pathways, could lead to better remedies for insomnia and more effective anaesthetic drugs.
Scientists from Imperial College London found that certain types of sedative drugs work by 'switching on' neurons in a particular area of the brain, called the preoptic hypothalamus.
Their work, in mice, showed that it is these neurons that are responsible for shutting down the areas of the brain that are inactive during deep sleep.
Following a period of sleep deprivation, the brain triggers a process that leads to a deep recovery sleep. The researchers found that the process that is triggered by the sedatives is very similar.
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The knowledge that one distinct area of the brain triggers this kind of deep sleep paves the way for the development of better targeted sedative drugs and sleeping pills.
These new drugs could directly hijack this natural mechanism to work more effectively, with fewer side effects and shorter recovery times.
"If you don't sleep for a long period, your body shuts down - almost as if you had taken a drug," said study co-author Professor Bill Wisden, from the Department of Life Sciences at Imperial College London.
"Although we know that certain sedatives are effective, there are lots of gaps in scientists' knowledge in terms of precisely what sedatives are doing in the brain," said Nick Franks, also from the Department of Life Sciences at Imperial College London.
"We looked at the class of sedative drugs commonly used for patients undergoing investigative procedures or minor operations, to try and identify the circuitry in the brain that they are affecting.
"What we found was really striking. Most people might think that sedative drugs would work by directly shutting down certain neural pathways but actually what happened was that they first switched on one particular area - the preoptic hypothalamus - and this then caused other parts of the brain to shut down," Franks said.
When the researchers subsequently targeted those neurons in the mice with a selective chemical, this was sufficient to produce a recovery sleep in the mice.