People often experience headaches and body pain after a lack of sleep, but the mechanisms behind this phenomenon are unclear. A new study led by investigators at Massachusetts General Hospital and published in Nature Communications reveals that a certain chemical messenger, or neurotransmitter, plays a major role.

Through experiments conducted in mice, the researchers found that the heightened pain sensitivity that can result from chronic sleep disruption—or chronic sleep disruption-induced hyperalgesia—involved signaling from a part of the brain known as the thalamic reticular nucleus.

Analyses of metabolites showed that the level of N-arachidonoyl dopamine, a type of neurotransmitter called an endocannabinoid, decreased in the thalamic reticular nucleus as a result of sleep deprivation.

Activity of the cannabinoid receptor 1, which is involved in controlling pain perception, also decreased in the thalamic reticular nucleus after chronic sleep disruption.

Administering N-arachidonoyl dopamine to the thalamic reticular nucleus reduced chronic sleep disruption-induced hyperalgesia in mice.

This beneficial effect of administered N-arachidonoyl dopamine could be countered by blocking the cannabinoid receptor 1, suggesting that both the receptor and N-arachidonoyl dopamine play a role in pain sensitivity due to sleep deprivation.

“We provide a mechanism as to how sleep disruption leads to exaggerated pain, suggesting that harnessing the endocannabinoid system might break the vicious cycle between pain and sleep loss,” says co–senior author Shiqian Shen, MD, the clinical director of Massachusetts General Hospital’s Tele Pain Program, in a release.

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