Following a lack of sleep, individuals commonly experience headaches and bodily discomfort, yet the precise underlying mechanisms remain elusive. A recent study, spearheaded by researchers at Massachusetts General Hospital (MGH), a founding member of Mass General Brigham (MGB) and published in Nature Communications, sheds light on the pivotal role played by a specific chemical messenger, or neurotransmitter.
Through experiments conducted on mice, the scientists discovered that heightened pain sensitivity resulting from chronic sleep disruption (CSD), also known as CSD-induced hyperalgesia, was linked to signaling from a region of the brain called the thalamic reticular nucleus (TRN).
Metabolite analyses revealed a decrease in the level of N-arachidonoyl dopamine (NADA), a type of neurotransmitter known as an endocannabinoid, in the TRN due to sleep deprivation. Additionally, the activity of the cannabinoid receptor 1, which regulates pain perception, diminished in the thalamic reticular nucleus after CSD.
Administering NADA to the TRN alleviated CSD-induced hyperalgesia in mice. Interestingly, this positive effect of administered NADA could be counteracted by blocking the cannabinoid receptor 1, indicating that both the receptor and NADA contribute to heightened pain sensitivity resulting from sleep deprivation.
Co-senior author Shiqian Shen, MD, the clinical director of MGH’s Tele Pain Program, emphasizes, “We elucidate a mechanism by which sleep disruption leads to heightened pain, suggesting that manipulating the endocannabinoid system could disrupt the cycle between pain and sleep loss.
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