Bored and Sleepy
A trader in the Standard & Poor's 500 stock index options pit at the Chicago Board Options Exchange yawns as he reacts to the Federal Reserves interest rate hike, Dec. 16, 2015. Joshua Lott/Getty Images

Depending on your personal idea of fun things to do, the flip side of excitement — boredom — is always lurking in the shadows, and occasionally, all of us suffer from its pangs that bring with them the desire to sleep. And while it is a feeling that is familiar to everyone, it is only now that science is discovering the mechanism that links boredom with its soporific effects.

But what is boredom itself? Mark Fenske, a professor of psychology at the University of Guelph, Canada, who co-authored a 2012 paper that attempted a scientific definition of the term, said in a statement at the time: “At the heart of it is our desire to engage with the world or some other mental activity, and that takes attention. When we cannot do this — that seems to be what leads to frustration and the aversive state we call ‘boredom’.”

Your own personal experiences of being bored may not necessarily fit the precise (though still generic) criteria laid down by Fenske, but it turns out that the sleep-inducing aspect of boredom is linked to the same part of the brain that is associated with motivation, pleasure and positive reinforcement.

In an open-access study published Friday in the journal Nature Communications, a group of researchers from Belgium, China and Japan try to shed light on the neural systems in the brain that affect “sleep/wake behavior” as “influenced by cognitive and emotional factors.”

The region of the brain the researchers focused on is called nucleus accumbens. There is one in each cerebral hemisphere, and they are located in the basal forebrain in humans. The researchers conducted their tests on mice, using “chemo-genetic and optical techniques to remotely control the activities of nucleus accumbens neurons and the behaviors they mediate.”

The neurons of nucleus accumbens were found to have significant ability to induce slow-wave sleep, which is characterized by high-voltage slow brain waves and accounts for the majority of our natural sleep. According to the researchers, this behavior of the nucleus accumbens neurons could be caused by a neuromodulator called adenosine.

“The classic somnogen adenosine is a strong candidate for evoking the sleep effect in the nucleus accumbens,” Yo Oishi from the University of Tsukuba, co-lead author of the study, said in a statement Friday.

Oishi explained that a specific type of adenosine receptors, called A2A receptors, are expressed densely in the nucleus accumbens, the inhibition of which is what makes caffeine — “the most widely consumed psychostimulant in the world” — produce its awakening effect. It was these receptors that researchers activated or suppressed in mice, while also looking for receptor activity when the mice were engaged in stimulating or non-stimulating tasks.

The researchers concluded: “Compounds that activate A2A receptors in the nucleus accumbens may open safe therapeutic avenues for treating insomnia, which is one of the most common sleep problems with an estimated prevalence of 10-15 percent in the general population and 30-60 percent in the older population.”

Other universities whose researchers were involved in the study are Shanghai Medical College of Fudan University and Anhui Medical University from China, and Université Libre de Bruxelles, Belgium. The paper is titled “Slow-wave sleep is controlled by a subset of nucleus accumbens core neurons in mice.”