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Cannabinoid-2 Agonism with AM2301 Mitigates Morphine-Induced Respiratory Depression
Beth M Wiese1, Erika Liktor-Busa1, Aidan Levine1
1Department of Pharmacology, University of Arizona, Tucson, Arizona, USA.
Cannabis and Cannabinoid Research
|May 17, 2021
Summary
Cannabinoid receptor activation impacts opioid-induced respiratory depression. Selective activation of cannabinoid-2 receptors (CB2R) may offer a novel therapeutic strategy to mitigate opioid overdose deaths.
Area of Science:
- Neuroscience
- Pharmacology
- Respiratory Physiology
Background:
- Opioid overdose deaths, primarily due to respiratory depression, remain a critical public health issue.
- Opioid-induced respiratory depression originates in the brainstem's preBötzinger complex, decreasing reflexive breathing.
- The role of cannabinoid receptors (CB1R and CB2R) in modulating opioid-induced respiratory depression is not well understood.
Purpose of the Study:
- To investigate the effects of cannabinoid receptor agonism on opioid-induced respiratory depression.
- To determine the specific roles of cannabinoid-1 receptors (CB1R) and cannabinoid-2 receptors (CB2R) in this process.
Main Methods:
- Male mice were treated with selective CB1R and CB2R agonists, alone and with morphine.
- Respiratory depression was assessed using whole-body plethysmography.
- The effects of agonists on morphine-induced respiratory depression were quantified.
Main Results:
- Nonselective CB1R/CB2R agonists and a selective CB1R agonist induced respiratory depression.
- Selective CB2R agonists did not induce respiratory depression.
- A selective CB2R agonist significantly attenuated morphine-induced respiratory depression.
Conclusions:
- Activation of CB2R, but not CB1R, is key to mitigating opioid-induced respiratory depression.
- Selective CB2R agonists show potential as adjunctive therapies to prevent opioid overdose.
Keywords:
cannabinoid receptor 1cannabinoid receptor 2mu opioid receptoropioid-induced respiratory depressionpreBötzinger complexMore Related Videos
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