Discussione:Endocannabinoidi
Help
Qualcuno vuole dare una mano a completare la bibliografia, utilizzando il pattern delle prime voci?
Vale a dire:
Autori, Titolo (in corsivo), Rivista, Link (eventuale) ad Abstract o Full-text
Grazie! Esculapio 01:50, 15 nov 2005 (CET)
Stuff 1
File:Http://www.mult-sclerosis.org/news/Apr2003/CannabisFig3.jpg Figure 3. Endocannabinoid agonism—degradation pathway. Endocannabinoids are formed within neurons and other cell types via multiple biosynthetic pathways (1). Rather than being stored as active molecules these are produced “on demand” from membranous fatty-acid precursors via the activity of phosphodiesterase (PDE) enzymes such as phospholipase D (anandamide) and phospholipase C (2-AG). This process occurs (2) after cellular stimulation by signals such as neuronal depolarisation (Ca2+ influx) to cause the extracellular release of active endocannabinoids (3). After release, the endocannabinoid can either bind cannabinoid receptors (agonism pathway) or be degraded. After receptor binding (4) the receptor signals the second messenger systems (eg, reducing adenylate cyclase and for CB1 inhibiting Ca2+ channels or stimulating inwardly rectifying K+ channels) that signal the cannabimimetic activities (5). There is also a degradation pathway expressed on either receptor bearing or other cells. The endocannabinoids are degraded through reuptake by a diffusion facilitated transport molecule (6) and then hydrolytically cleaved by enzymes (7) such as fatty-acid-amide hydrolase to break down the endocannabinoids to molecules such as arachidonic acid and ethanolamine.
