People often experience headaches and body pain after a lack of sleep, but the mechanisms behind this phenomenon are unclear. A new study published in Nature Communications reveals that a certain endocannabinoid neurotransmitter plays a major role.
The animal-based study, led by investigators at Massachusetts General Hospital (MGH), a founding member of Mass General Brigham (MGB), found that the heightened pain sensitivity than can result from chronic sleep disruption (CSD) – or CSD-induced hyperalgaesia – involved signalling from a part of a brain known as the thalamic reticular nucleus (TRN).
Analyses of metabolites showed that the level of N-arachidonoyl dopamine (NADA), a type of neurotransmitter called an endocannabinoid, decreased in the TRN 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 CSD.
Administering NADA to the TRN reduced CSD-induced hyperalgaesia in mice.
This beneficial effect of administered NADA could be countered by blocking the cannabinoid receptor 1, suggesting that both the receptor and NADA 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 MGH’s Tele Pain Program.
Source: Massachusetts General Hospital
