How do we fall asleep and wake up? Scientists uncover key mechanism

INSOMNIA, jet lag, seasonal affective disorder – new treatments could be in the cards for all of these circadian rhythm-related conditions, after researchers have uncovered a neurobiological pathway that plays a key role in falling asleep and waking up. Published in the journal Nature Communications, the study suggests that BK channels in the suprachiasmatic nucleus (SCN) – located in the hypothalamus of the brain – regulate the “switch” between sleep and wakefulness.
BK channels are part of the ion channel family. In the brain, they are responsible for conducting electrical current, enabling communication between neurons, or brain cells. According to study co-author Prof. Andrea Meredith – of the University of Maryland School of Medicine – and colleagues, these channels are particularly active in the SCN, which is the brain region involved in the regulation of circadian rhythms; it tells us when to go to sleep, how long to sleep for and when to get up.
Unfortunately, some people’s circadian rhythm, or body clock, is out of sync, which can lead to sleep disorders, such as insomnia, jet lag and seasonal affective disorder. To find out if BK channels in the SCN play a role in circadian rhythm, Prof. Meredith and colleagues analysed the SCN of mice. The sleep pattern of mice is opposite to that of humans; they sleep during the day but stay awake at night.
Some of the mice analyzed had been genetically modified so that their BK channels in the SCN could not be inactivated. In order to record activity in the BK channels of these mice – as well as the BK channel activity of normal mice – the team implanted electrodes in SCN neurons of the rodents. Among normal mice, the team found that during the day, when the rodents sleep, the BK channels were inactive, but they were active during nighttime, when mice are normally awake.
An inactive daytime BK channel triggered higher neuronal activity in the SCN of mice, which led to sleep, but an active nighttime BK channel reduced neuronal activity, triggering wakefulness. The team reached this conclusion after identifying lower neuronal activity in the mice that were unable to inactivate their BK channels, which they found led to increased daytime wakefulness.
The researchers note that, despite mice having an opposite sleep pattern to us, the association between neuronal activity and sleep-wake cycles is similar in both mice and humans. According to the team, this study is the first to show that inactivation of BK channels is key for encoding the brain’s circadian rhythm, regulating sleep-wake cycles.
Previously, studies have suggested that the number of ion channels present on the surface of SCN cells is responsible for neuronal activity that regulates circadian rhythm. This latest research, however, shows that it is the activation – and inactivation – of BK channels that is responsible.

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