dehydrovomifoliol and Disease-Models--Animal

Some cannabinoids have been shown to suppress chronic pain by targeting glycine receptors (GlyRs). Although cannabinoid potentiation of α3 GlyRs is thought to contribute to cannabinoid-induced analgesia, the role of cannabinoid potentiation of α1 GlyRs in cannabinoid suppression of chronic pain remains unclear. Here we report that dehydroxylcannabidiol (DH-CBD), a nonpsychoactive cannabinoid, significantly suppresses chronic inflammatory pain caused by noxious heat stimulation. This effect may involve spinal α1 GlyRs since the expression level of α1 subunits in the spinal cord is positively correlated with CFA-induced inflammatory pain and the GlyRs antagonist strychnine blocks the DH-CBD-induced analgesia. A point-mutation of S296A in TM3 of α1 GlyRs significantly inhibits DH-CBD potentiation of glycine currents (I

Topics: Action Potentials; Analgesics; Animals; Animals, Genetically Modified; Cannabinoids; Cyclohexanones; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Freund's Adjuvant; Gene Expression Regulation; Glycine Agents; HEK293 Cells; Humans; In Vitro Techniques; Inflammation; Male; Mice; Mice, Inbred C57BL; Mutation; Neurons; Pain; Pain Measurement; Patch-Clamp Techniques; Receptors, Glycine; Reflex, Startle; Rotarod Performance Test; Spinal Cord; Strychnine; Time Factors; Transfection