When a particular area of the brain called the preoptic hypothalamus is switched on chemically, it triggers a deep sleep, according to scientists at Imperial College London in a new mouse study.
The action is very similar to the way that sedatives work on the brain, and the new findings eventually may lead to better treatments for insomnia and more effective anesthetic drugs.
“Lack of sleep is a really serious problem for many people, such as people suffering from stress or people working irregular shifts, and it affects their physical and mental health,” said study co-author Professor Bill Wisden.
“There are many different sleeping pills available but none of them provide rest that is as restorative as natural sleep. We hope that our new research will ultimately lead to new ways of addressing this problem.”
After experiencing sleep deprivation, the brain triggers a mechanism that leads to a deep recovery sleep. The researchers found that this process is very similar to the work of sedative drugs.
In mice, when the scientists chemically activated specific neurons in the preoptic hypothalamus, it triggered a recovery sleep in the animals.
“If you don’t sleep for a long period, your body shuts down, almost as if you had taken a drug,” said Wisden. “We’ve shown that sedative drugs trigger the same neurons, making the two types of unconsciousness very similar.”
These findings have important implications because although scientists understand how sedatives bind to certain receptors to cause their desired effects, it had previously been assumed that they had a general effect throughout the brain.
Knowing that one particular area of the brain triggers this kind of deep sleep could pave the way for the development of better targeted sedative drugs and sleeping pills with fewer side effects and shorter recovery times.
“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. 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,” said Nick Franks, Ph.D., also from the Department of Life Sciences at Imperial College London.
“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.”
The team plan to continue their investigations into sleep induction in the brain, to try to understand more of the complex chemical circuitry governing our response to tiredness.
Source: Imperial College London