Because CB1 receptor agonists decrease nociceptive DRG neuronal activity,45,53–55 it has been proposed that activation of these receptors will inhibit nociceptive afferents in the dorsal horn, resulting in dampened pain transmission.56 However, a recent study showed that analgesia produced by spinal administration of ∆9-THC was dependent on Cav3.2 T-type channels and not CB1 or CB2 receptors in male mouse models of inflammatory and neuropathic pain.57 Thus, whether cannabis components mediate analgesia partially through the activation of spinal CB1 receptors remains an open question. This evidence concerns the gene CNR1 and neuropathic pain.