Cannabidiol attenuates chemotherapy-induced peripheral neuropathic pain through a mechanism that requires the enzyme N-acylphosphatidylehtanolamine-specific phospoholipase D (NAPE-PLD)

This dataset contains behavioral and pharmacological data generated from studies investigating the mechanisms underlying the analgesic effects of cannabidiol (CBD) in a mouse model of chemotherapy-induced peripheral neuropathy (CIPN). CBD is a non-psychoactive constituent of cannabis that has demonstrated therapeutic potential for chronic neuropathic pain, but the biological pathways mediating its effects remain incompletely understood. The studies evaluated both acute and chronic antinociceptive effects of CBD in paclitaxel-induced CIPN. Behavioral assessments of mechanical and cold hypersensitivity were conducted in wild-type mice as well as mice with targeted deletions of N-acyl phosphatidylethanolamine phospholipase D (NAPE-PLD) or G protein-coupled receptor 55 (GPR55). Pharmacological experiments examined the contribution of cannabinoid receptors (CB1 and CB2) and peroxisome proliferator-activated receptors (PPARα and PPARγ) using selective receptor antagonists. The dataset includes measures of neuropathic pain-related behaviors following CBD administration, receptor antagonist treatments, and repeated dosing paradigms during both the development and maintenance phases of paclitaxel-induced neuropathy. Data demonstrate that CBD suppresses chemotherapy-induced behavioral hypersensitivities through mechanisms dependent on NAPE-PLD and PPAR signaling pathways, while GPR55 is not required for CBD-mediated antinociception. These data support the conclusion that NAPE-PLD and PPAR receptors play critical roles in the analgesic actions of CBD in chemotherapy-induced neuropathic pain and provide a resource for investigating lipid-mediated signaling mechanisms in pain modulation.