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The endocannabinoid N-arachidonoyl dopamine is critical for hyperalgesia induced by chronic sleep disruption.
Ding, Weihua; Yang, Liuyue; Shi, Eleanor; Kim, Bowon; Low, Sarah; Hu, Kun; Gao, Lei; Chen, Ping; Ding, Wei; Borsook, David; Luo, Andrew; Choi, Jee Hyun; Wang, Changning; Akeju, Oluwaseun; Yang, Jun; Ran, Chongzhao; Schreiber, Kristin L; Mao, Jianren; Chen, Qian; Feng, Guoping; Shen, Shiqian.
Afiliação
  • Ding W; Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Yang L; Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Shi E; Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Kim B; Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Low S; Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Hu K; Department of Pathology, Tuft University School of Medicine, Boston, MA, USA.
  • Gao L; Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Chen P; College of Science and Mathematics, University of Massachusetts Boston, Boston, MA, USA.
  • Ding W; College of Science and Mathematics, University of Massachusetts Boston, Boston, MA, USA.
  • Borsook D; Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Luo A; Summer Intern Program of the Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, currently at Brandeis University, Boston, MA, USA.
  • Choi JH; Center for Neuroscience, Korea Institute of Science and Technology, Seoul, South Korea.
  • Wang C; Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Akeju O; Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Yang J; Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Ran C; Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Schreiber KL; Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
  • Mao J; Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Chen Q; McGovern Institute for Brain Research and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
  • Feng G; Zhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
  • Shen S; McGovern Institute for Brain Research and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA. fengg@mit.edu.
Nat Commun ; 14(1): 6696, 2023 10 25.
Article em En | MEDLINE | ID: mdl-37880241
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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Limite: Animals Idioma: En Ano de publicação: 2023 Tipo de documento: Article
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Limite: Animals Idioma: En Ano de publicação: 2023 Tipo de documento: Article