Organizers: Charles Lunn, Schering-Plough; and Dale Deutsch, Stony Brook University
The therapeutic value of the cannabinoid system has been a topic of increasing scientific debate/interest in recent years. In addition to the anecdotal evidence that smoked marijuana treatments can moderate pain, positive phase III clinical trials have demonstrated the efficacy of marijuana extracts on the symptoms of multiple sclerosis and neuropathic pain [Sativex (organic plant extract containing delta-9-tetrahydrocannabinol and cannabidiol); GW Pharmaceuticals]. In addition, clinical trials of a compound specific for the cannabinoid CB1 receptor [Acomplia (rimonibant); Sanofi Aventis] continues to show significant positive effects on obesity and on other obsessive disorders.
Recognizing the increasing appreciation of the therapeutic potential of the cannabinoid system, we will discuss the biology of the endogenous ligands for the cannabinoid receptors, the endocannabinoids, as potential therapeutic targets. The symposium will include a discussion of the metabolism of the endocannabinoid anandamide by the fatty acid acylhydrolase (FAAH) and in situ imaging studies showing how inhibiting the activity of this enzyme alters endocannabinoid distribution in the brain. Biology presentations will demonstrate that inhibiting FAAH activity can alter memory in mice. Finally, we will discuss the peripheral effects of modulating endocannabinoids, specifically as they influence pain and immune functions.
Dale Deutsch, "Biosynthesis and Degradation of Anandamide, and Endogenous Ligands of the Cannabinoid Receptors."
Sherrye Glaser, "Imaging the Regional Inhibition of Fatty Acid Amide Hydrolase (FAAH) Activity in the Mouse Brain."
2:40–3:00 Coffee Break
Aron Lichtman, "FAAH-Getting: Evidence for a Role of the Endocannabinoid System in Extinction Processes."
Norbert E. Kaminski, "Endocannabinoid-Induced Suppression of Interleukin-2 Involves Cyclooxygenase-2, Is Mediated in Part Through a Nuclear Receptor, and Occurs Independently of CB1 and CB2."
4:35–4:450 Closing Remarks