Cannabidiol increases the nociceptive threshold in a preclinical model of Parkinson's disease.

摘要: Medications that improve pain threshold can be useful in the pharmacotherapy of Parkinson's disease (PD). Pain is a prevalent PD's non-motor symptom with higher prevalence analgesic drugs prescription for patients. However, specific therapy PD-related are not available. Since endocannabinoid system expressed extensively different levels pathway, designed to target this have promising therapeutic potential modulation pain. Thus, we examined effects 6-hydroxydopamine- induced PD on nociceptive responses mice and influence cannabidiol (CBD) 6-hydroxydopamine-induced nociception. Further, investigated pathway involved effect CBD through co-administration fatty acid amide hydrolase (FAAH) inhibitor, increasing endogenous anandamide levels, possible targets from anandamide, i.e., cannabinoid receptors subtype 1 2 (CB1 CB2) transient receptor vanilloid type (TRPV1). We report parkinsonism decreases thermal mechanical threshold, whereas (acute chronic treatment) reduces hyperalgesia allodynia evoked by 6-hydroxydopamine. Moreover, ineffective doses either FAAH inhibitor or TRPV1 antagonist potentialized CBD-evoked antinociception while an inverse agonist CB1 CB2 prevented antinociceptive CBD. Altogether, these results indicate drug prevent parkinsonism-induced reduction. They also suggest important CBD-induced analgesia could produce levels.