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.
    
In mice, when the researchers used a chemical to activate only specific neurons in the preoptic hypothalamus, this produced a recovery sleep in the animals.
    
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.

In the study, published in the journal Nature Neuroscience, the researchers used a genetic tagging system to mark neurons in mice that were activated both during sedation and in recovery sleep.
    
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.

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