The endocannabinoid N-arachidonoyl dopamine is critical for hyperalgesia induced by chronic sleep disruption

Weihua Ding, Liuyue Yang, Eleanor Shi, Bowon Kim, Sarah Low, Kun Hu, Lei Gao, Ping Chen, Wei Ding, David Borsook, Andrew Luo, Jee Hyun Choi, Changning Wang, Oluwaseun Akeju, Jun Yang, Chongzhao Ran, Kristin L. Schreiber, Jianren Mao, Qian Chen, Guoping Feng () and Shiqian Shen ()
Additional contact information
Weihua Ding: Harvard Medical School
Liuyue Yang: Harvard Medical School
Eleanor Shi: Harvard Medical School
Bowon Kim: Harvard Medical School
Sarah Low: Harvard Medical School
Kun Hu: Tuft University School of Medicine
Lei Gao: Harvard Medical School
Ping Chen: University of Massachusetts Boston
Wei Ding: University of Massachusetts Boston
David Borsook: Harvard Medical School
Andrew Luo: currently at Brandeis University
Jee Hyun Choi: Korea Institute of Science and Technology
Changning Wang: Harvard Medical School
Oluwaseun Akeju: Harvard Medical School
Jun Yang: Harvard Medical School
Chongzhao Ran: Harvard Medical School
Kristin L. Schreiber: Harvard Medical School
Jianren Mao: Harvard Medical School
Qian Chen: Massachusetts Institute of Technology
Guoping Feng: Massachusetts Institute of Technology
Shiqian Shen: Harvard Medical School

Nature Communications, 2023, vol. 14, issue 1, 1-13

Abstract: Abstract Chronic pain is highly prevalent and is linked to a broad range of comorbidities, including sleep disorders. Epidemiological and clinical evidence suggests that chronic sleep disruption (CSD) leads to heightened pain sensitivity, referred to as CSD-induced hyperalgesia. However, the underlying mechanisms are unclear. The thalamic reticular nucleus (TRN) has unique integrative functions in sensory processing, attention/arousal and sleep spindle generation. We report that the TRN played an important role in CSD-induced hyperalgesia in mice, through its projections to the ventroposterior region of the thalamus. Metabolomics revealed that the level of N-arachidonoyl dopamine (NADA), an endocannabinoid, was decreased in the TRN after CSD. Using a recently developed CB1 receptor (cannabinoid receptor 1) activity sensor with spatiotemporal resolution, CB1 receptor activity in the TRN was found to be decreased after CSD. Moreover, CSD-induced hyperalgesia was attenuated by local NADA administration to the TRN. Taken together, these results suggest that TRN NADA signaling is critical for CSD-induced hyperalgesia.

Date: 2023
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DOI: 10.1038/s41467-023-42283-6

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