Understanding the Link Between Sleep Deprivation and Pain Sensation
Frequently, individuals encounter headaches and bodily discomfort when they're sleep-deprived, yet the precise mechanisms responsible for this occurrence remain uncertain. A recent research sheds light on the significant involvement of a particular neurotransmitter called endocannabinoid ().
Through experiments conducted in mice, the researchers found that the heightened pain sensitivity than can result from chronic sleep disruption (CSD)-or CSD-induced hyperalgesia-involved signaling from a part of a brain known as the thalamic reticular nucleus (TRN).
‘The concentration of N-arachidonoyl dopamine (NADA), categorized as an endocannabinoid neurotransmitter, diminished within the thalamic reticular nucleus (TRN) due to the effects of sleep deprivation. #pain #sleepdeprivation #neurotransmitter’
Activity of the cannabinoid receptor 1, which is involved in controlling pain perception, also decreased in the thalamic reticular nucleus after CSD.
The research was spearheaded by researchers from Massachusetts General Hospital (MGH), a founding member of Mass General Brigham (MGB), and featured in the journal Nature Communications.
Applying NADA to the TRN Alleviated CSD-Induced Hyperalgesia 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.
Reference:
- The endocannabinoid N-arachidonoyl dopamine is critical for hyperalgesia induced by chronic sleep disruption - (https:www.nature.com/articles/s41467-023-42283-6)
Source: Eurekalert