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Cannabinoids such as Δ9-tetrahydrocannabinol (THC), which act on CB1 and CB2 receptors, improve neuropathic pain and medication-induced nausea. However, these cannabinoids' effects on CB1 receptors cause physical dependence and psychological adverse effects. In a rodent study, researchers examined the pharmacologic and clinical actions of a selective CB2 agonist (AM1710) in neuropathic pain and hyperesthesia that were induced by the chemotherapy drug paclitaxel.
In wild-type mice, THC suppressed paclitaxel-induced allodynia but was associated with cannabinoid tolerance and with motor and autonomic adverse effects; a CB1 antagonist precipitated THC withdrawal symptoms. Systemic or intrathecal AM1710 reversed allodynia in wild-type mice and CB…