Journal
CANNABIS AND CANNABINOID RESEARCH
Volume 6, Issue 5, Pages 401-412Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/can.2020.0076
Keywords
cannabinoid receptor 1; cannabinoid receptor 2; mu opioid receptor; opioid-induced respiratory depression; preBö tzinger complex
Categories
Funding
- National Institutes of Health/National Institute of Drug Abuse [1P01DA041307-01, DA 009158, DA 045020, DA 05801, DA 041307]
- National Cancer Institute [R01CA142115-02]
- Comprehensive Pain and Addiction Center (CPAC)
- University of Arizona Health Sciences
- NIH [S10 OD019948]
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The study found that activation of the cannabinoid receptor 2 (CB2R) significantly reduces opioid-induced respiratory depression, supporting the potential use of selective CB2R agonism as an adjunct therapy for opioids.
Introduction: An escalating number of fatalities resulting from accidental opioid overdoses typically attributed to respiratory depression continue to define the opioid epidemic. Opioid respiratory depression results from a decrease in reflexive inspiration within the preBotzinger complex in the brainstem. Objective: Cannabinoid receptor agonism is reported to enhance opioid analgesia, yet whether cannabinoids enhance or inhibit opioid-induced respiratory depression is unknown. Methods: Studies herein sought to define the roles of cannabinoid-1 receptor (CB1R) and cannabinoid-2 receptor (CB2R) on respiratory depression using selective agonists alone and in combination with morphine in male mice. Results: Using whole body plethysmography, the nonselective CB1R and CB2R agonist (Delta(9)-tetrahydrocannabinol) and the CB1R synthetic cannabinoid, AM356, induced respiratory depression, whereas the well-published selective CB2 agonist, JWH 133, and the novel CB2 agonist (AM2301) did not. Moreover, a selective CB2R agonist (AM2301) significantly attenuated morphine sulfate-induced respiratory depression. Conclusion: Notably, findings suggest that attenuation of opioid-induced respiratory depression relies on CB2R activation, supporting selective CB2R agonism as an opioid adjunct therapy.
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