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Decoded: How we fall asleep and wake up

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Decoded: How we fall asleep and wake up

New York - Inactivation of potassium channel is a critical neurobiological process for regulating sleep and wakefulness cycles.

Published: Sun 17 Apr 2016, 2:32 PM

Updated: Sun 17 Apr 2016, 4:42 PM

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  • IANS

Scientists have identified a new mechanism in the human brain that plays a major role in regulating the "switch" between sleep and wakefulness.
The researchers focused on a particular brain area, the suprachiasmatic nucleus (SCN) in the hypothalamus, which acts as the brain's internal clock and plays a crucial role in determining when we fall asleep and when we wake up.
The findings showed that inactivation of potassium channels known as BK in SCN are critical for encoding the 24-hour human biological cycle.
Inactivation of potassium channel is a critical neurobiological process for regulating sleep and wakefulness cycles.
An inactivation of these channels means individuals may find it harder to fall asleep.
"We knew that BK channels were widely important throughout the body. But now we have strong evidence that they are specifically and intrinsically involved in the wake-sleep cycle. That's really exciting," said Andrea Meredith, associate professor at University of Maryland School of Medicine in US.
Further, these potassium channels form an inherent part of the sleep-wakefulness process and are important for activating muscles, and play a prominent role in controlling blood pressure, heart rate and bladder function.
The study, which appeared in Nature Communications was conducted on two groups of mice.
 Image credit: Andrea Meredith
While, the first group was normal, the second was genetically modified so that the potassium channels remained inactivated.
With the use of electrodes placed on the SCN neurons, the team measured activity in these channels and followed the animals' sleep.
They discovered that in the genetically altered group, the impossibility to inactivate BK channels lead to more wakefulness during the day, when the mice were actually supposed to be asleep.
The new understanding of the inactivation mechanism could potentially be used to develop drugs to treat sleep disorders, jet lag, and seasonal affective disorder, all of which involve problems with the SCN circadian clock, the researchers suggested.
 



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