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“A mechanistic explanation for that wasn’t appreciated before,” Foster says. Nocturnal species such as mice are the opposite: Light exposure at dusk delays wakefulness substantially, whereas at dawn it brings on sleep a bit sooner ( see the phase response curve in the image below, top panel). Diurnal species experience big delays in our sleep-wake cycles when exposed to light at dawn, and small advances at dusk. This master clock in turn regulates through molecular signaling many aspects of the clock system in various tissues throughout the body.Īnimals are particularly sensitive to light at dawn and dusk, when exposure to light can delay or advance our sleep-wake cycle-a trait that we can use to help alleviate jetlag ( see “Adapting Your Body Clock to a 24-Hour Society” November–December 2017). These nerve cells send signals to turn on key genes called Per1 and Per2 in the brain’s “master clock,” the suprachiasmatic nuclei. Light entrains this clock system when it is detected by specialized nerves in the eye, called photosensitive retinal ganglion cells, which were first identified in 2002, setting off a flurry of research on light entrainment over the following two decades. We all have a built-in clock system that keeps our sense of time and determines when we are active and when we are sleepy. This interdisciplinary realm of research spanning the team members’ careers has led them to the realization that the sleep-wake system draws from all the key neurotransmitter systems, and that the sleep-wake cycle is a global brain event. In the process, the researchers discovered a drug that may mimic the effects of light exposure, with potential applications to health problems ranging from sleep dysfunction after eye injuries to schizophrenia. But until recently, no one had determined how adenosine made that happen.Ī study published in Nature Communications in April, led by neuroscientist Aarti Jagannath, circadian biologist Russell Foster, and pharmacologist Sridhar Vasudevan, all at Oxford University, marks a major advance in untangling the roles of adenosine and light in sleep. As an animal uses energy while it is awake, adenosine builds up in the body-for example, through the breakdown of a key metabolic molecule, adenosine triphosphate (ATP)-and induces a sense of sleepiness. Sleep researchers have also known that caffeine delays sleep by blocking the action of a molecule called adenosine. Circadian biologists have long been aware that exposure to light can shift a mammal’s sleep-wake cycle, but they haven’t been able to work out why light exposure becomes ineffectual when an animal is sleep-deprived. Until recently, though, no one understood the exact molecular mechanisms responsible for this ubiquitous experience. At one point or another, we’ve all hit the wall of sleep: the point when you are so exhausted that you cannot stay awake, no matter how bright it is outside or how much caffeine you have consumed.