How we fall asleep and wake up decoded

Researchers have identified a pathway in the brain that appears to play a key role in regulating the "switch" between wakefulness and sleep, a finding which could lead to better treatments for insomnia and jet lag. Researchers from the University of Maryland School of Medicine (UM SOM) in the US focused on a particular brain area, the suprachiasmatic nucleus in the hypothalamus. This region acts as the brain's internal clock, determining when we feel like going to sleep, how long we sleep, and when we feel like getting up, researchers said. Within the suprachiasmatic nucleus (SCN), they focused on certain ion channels, proteins that conduct electrical current, relaying information from one neuron to another. Researchers also focused on a group of channels known as BK potassium channels, which seem to be particularly active in the SCN. They examined mice, whose schedule is opposite to humans - they sleep during the day and are awake at night. Researchers found that BK channels are active during waking, which for the mice was at night; during the day the BK channels were inactive. In this daytime context, the role of the BK channels is to inhibit wakefulness, they said. Researchers examined normal mice, along with mice that had been genetically altered so that their BK channels could not be inactivated. They then recorded activity in these channels, via electrodes placed in SCN neurons. In the brains of the genetically modified group, the animals that could not inactivate their BK channels, they found lower levels of neuronal activity, which was associated with more daytime wakefulness. This was unusual, because mice generally sleep during the day, researchers said. "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," said Andrea Meredith from UM SOM. In the past, scientists had thought that the day-night pattern of firing was largely driven by a different mechanism, the number of ion channels that exist on the surface of SCN neurons. The new study shows that the key is not the number of channels, but the fact that the channels are being activated, and more importantly, inactivated, at specific times of day, researchers said. The discovery has clinical implications. The new understanding of the inactivation mechanism could potentially be used to develop drugs that target circadian rhythms. Such a medication could be used to treat sleep disorders, jet lag, and seasonal affective disorder, all of which involve problems with the SCN circadian clock, Meredith said. The findings were published in the journal Nature Communications.