Host: The Japanese Pharmacological Society, The Japanese Society of Clinical Pharmacology
Name : WCP2018 (18th World Congress of Basic and Clinical Pharmacology)
Location : Kyoto
Date : July 01, 2018 - July 06, 2018
Cannabis sativa preparations have probably been used since millennia for pain relief and are still an important part of our analgesic pharmacopeia. This presentation will summarize our current understanding about the analgesic mechanism of cannabinoids, from molecular mechanisms to the physiological effects. The psychoactive ingredient of C. sativa, 9-tetrahydrocannabinol (THC) activates two different G protein-coupled cannabinoid receptors, CB1 and CB2, both of which mediate different aspects of cannabinoid analgesic effects. CB2 receptors are mostly localized on immune cells and activated microglia. The analgesic effects of CB2 activation are mainly due to anti-inflammatory mechanisms, but probably also through the modulation of algogenic mediators. CB1 is prominently expressed in the central nervous system and is well-known as an important mediator of synaptic plasticity. Activation of CB1 on neurons modulates pain responses at different level, including the processing of nociceptive stimuli and the regulation of descending pain control systems. I will also show evidence that endocannabinoid signaling is involved in the modulation of the affective component of pain.
