Scientists at Stanford have identified a neural circuit crucial in sleep regulation patterns in mice, which could one day lead to better drugs and interventions for human insomnia.

Their study, published Monday in Nature Neuroscience, pinpoints for the first time the part of the mammalian brain where sleep patterns interact with machinery related to motivation and reward.

“Many people study motivation and many people study sleep, but actually there’s not much known about their link,” lead author Ada Eban-Rothschild tells Inverse. However, it makes intuitive sense that there should be a connection, given that our level of arousal certainly affects our motivation to sleep, or to get up in the morning. That’s what got Eban-Rothschild interested in investigating the question, she says.

This new insight was made possible in part by new technologies whereby specific neural circuits in genetically engineered lab mice can be activated, depressed, and monitored at will. For the study, Eban-Rothschild targeted the ventral tegmental area, or VTA, which is a bundle of nerve cells known to produce dopamine and ship it off to various locations in the brain. The VTA is a central part of reward and motivation systems, and is implicated in addictions, orgasms, love, and certain psychiatric disorders.

A mouse in an unfamiliar cage builds a nest in preparation for sleep.

Here’s what Eban-Rothschild found: When mice had activity in their VTA turned off, they were super into sleeping. Not even an attractive potential mate, tasty treats, or the scent of fox urine could rouse them from slumber for long. The opposite was true when she artificially switched the VTA on, and mice stayed up way past their bedtimes.

It’s not that the VTA-depressed mice were completely knocked out or drugged, though. Another experiment proved they were capable of staying awake. When she put the mice in an unfamiliar environment, the mice did not go to sleep right away, despite the lack of dopamine flooding their neural circuitry. Instead, they spent a good amount of time carefully assembling a nest from the available materials. Only when the nest was properly built did the critters put their little heads down for a snooze.

Usually, dopamine motivates action. In this case, it was the lack of dopamine that motivated the nest building behavior. This led Eban-Rothschild to the insight that perhaps the action of preparing for sleep might be quite important to the sleep itself. Even in familiar cages, the mice would go through a series of rituals before turning down — fixing the nest, eating, grooming, repeat.

It’s quite possible that many human sleep disorders could be prevented by paying more attention to how we prepare for bed. “Imagine building a nest,” suggests Eban-Rothschild. Certainly, it would be wise to avoid any stimulating activities that might result in a shot of dopamine to the brain close to bedtime.

Better understanding the neural connection between motivation and sleep could lead to better drugs to help with sleep, too, says Eban-Rothschild. Today, most sleeping pills target the entire brain, depressing activity in all areas. These might put you out, but the quality of sleep isn’t great, as it seems some of that neural activity is actually required for your brain to recuperate in the way it needs to.

What if a drug could target the VTA specifically — in just the right way at just the right time — allowing your brain to switch off but letting it do the rest of the work? The implications of that could be huge, both for sleep problems and psychiatric disorders, says Eban-Rothschild. But it’ll take some more work to get there.

“It’s really a strong association, but more research is needed,” she says. “This is just the beginning.”

Photos via Ada Eban-Rothschild/Stanford University School of Medicine