Scientists have identified
a protein molecule in the brains of fruit flies that they believe is the “switch” that controls the flies’ internal drive to sleep—and that a similar mechanism likely exists for human sleep
Researchers at the UK’s Oxford University Centre for Neural Circuits and Behaviour examined a small cluster of neurons in fruit flies that help to induce sleep. These neurons become active when flies are sleep deprived, and their increased activity stimulates an anesthetic response in the brain that sends the flies to sleep. A similar group of neurons with a similar pattern of activity exists in the human brain. These human neurons fire up when our bodies need sleep, and trigger a sedating response that helps usher us to sleep.
To pinpoint the molecular sleep switch in fruit flies’ brains, researchers manipulated genes associated with these sleep-inducing neurons. They found that when genes connected to a particular brain molecule were suppressed, these sleep-triggering neurons did not fire. Instead, the neurons remained quiet and flies were unable to sleep despite being significantly sleep deprived.
This discovery provides some important information that adds to our understanding of the body’s regulation of sleep. Sleep is driven by two different systems that function concurrently, one that takes its cues from our external environment, and the other that responds to the body’s internal sleep needs. The body’s circadian clock works in accordance with the 24-hour solar day and night. As night and darkness approach, circadian rhythms shift and initiate physiological changes—including the release of the sleep hormone melatonin—that prepare the body for rest and increase the inclination for sleep. Beginning in the early morning and continuing through much of the daylight hours, circadian rhythms promote alertness, diminishing the drive for sleep in order to promote a sustained period of wakefulness and activity during the day.
Our drive for sleep is also regulated by the body’s own sense of its need for rest. This internally-driven sleep system is known as sleep homeostasis. This system works much like a thermostat that regulates heat by sensing when temperatures dip too low or rise too high. The body’s homeostatic sleep mechanisms continually monitor how much sleep the body receives. When we go without sleep for a period of time, this system increases the drive for sleep. The longer we go without sleep, the more pressing our need for sleep becomes. Sleep homeostasis is influenced by both quantity and quality of sleep. Feeling tired and inclined to nod off after an abbreviated or restless night of sleep, or feeling uncontrollably drowsy after an unusually long day—these are signs of your homeostatic sleep drive cuing your brain and body to rest, in order to avoid a too-significant sleep deficit.
The circadian and homeostatic sleep systems work in concert to regulate our sleep and waking lives. When these two sleep systems are functioning normally and in sync with one another, we find ourselves with the energy and alertness we need during the day—and readiness to sleep at bedtime. Too often, however, our two sleep drives don’t work together as they should, and can find each other at odds. Circadian rhythms are highly sensitive and can easily be disrupted, leading to difficult and disrupted sleep—and stimulation of the internal drive to sleep at the “wrong” times. Nighttime exposure to artificial light is a significant and common hazard to healthy sleep function. In today’s endlessly lit-up and digital world, the very devices we rely on so heavily during our waking lives—smartphones, tablets, computers—can be detrimental to sleep and circadian function, in large part because of the particularly stimulating light they emit. People who perform shift work—irregular, rotating, and nighttime shifts that stray from the standard daytime work schedule—are at particularly high risk for disruptions to circadian rhythms, and the health problems associated with circadian dysfunction. So too are people who travel frequently and contend with jet lag.
Alterations to circadian function can interfere with the body’s homeostatic sleep system, making regular and restorative sleep patterns more difficult to achieve, and inhibiting daytime alertness and performance. The internal homeostatic sleep drive is a powerful one. Sleep deprivation—whether by disruptions to circadian function or other factors—elicits a strong corrective response in the body, as it seeks to restore balance to its sleep-wake equilibrium. Excessive daytime sleepiness, sleeping during the day, diminished focus, alertness and cognitive function are common symptoms of disordered and insufficient sleep—signs that the body’s sleep homeostasis is out of balance.
It may sound surprising that we’re just discovering the mechanism that controls the body’s internal—homeostatic—drive to sleep. In fact, there’s a great deal about the fundamental function and mechanisms of sleep that we don’t yet understand. This discovery of the brain’s homeostatic “sleep switch” is a significant step toward a more thorough understanding of how the human body’s drive for sleep really works. Deepening this understanding may improve existing sleep therapies and open important new avenues for treatment of sleep disorders. Researchers intend to further explore the behavior of these sleep-promoting neurons and the molecular switch that controls them, examining how the neurons behave during waking hours and what prompts the activation of the switch itself. Their discoveries may bring us closer to unlocking an essential and persistent mystery: the very purpose of sleep.
Michael J. Breus, PhD
The Sleep Doctor™
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