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The Neuroscientist Comments

It has been known for many centuries that cannabis has antiepileptic properties. The possibility that receptors for cannabis might be activated by endogenous ligands was suggested by the discovery that an anandamide and 2-arachidonoyl glycerol (2-AG) are both synthesized within mammals and bind to cannabinoid receptors including CB1, which is expressed within the brain. A number of studies have suggested that the expression of these “endocannabinoids” may increase as a result of various insults to the CNS and that they may have a neuroprotective effect. However, CB1 receptor-mediated neurotoxic effects have also been reported, and the putative neuroprotective effects of endocannabinoids have remained controversial. Now Marsicano and others (2003) have generated conditional mutant mice that lack expression of the CB1 receptor in principal forebrain neurons but not in nearby inhibitory interneurons, and they report that kainic acid induces excessive seizure activity in vivo in these knockouts. They observed that administration of kainic acid rapidly increased hippocampal levels of anandamide, which in turn protects neurons from excitotoxicity in wild-type principal hippocampal neurons but not in null-mutants. The authors suggest, on the basis of these observations, that an endogenous cannabinoid system provides on-demand protection against acute excitotoxicity. In an accompanying editorial, Mechoulam and Lichtman (2003) suggest that although endocannabinoids are important components of the brain’s firstline defense against excitotoxic damage, there may be important species differences. They also note that there appear to be parallels between the endocannabinoid system and the immune system and suggest that, similar to damage caused by inflammation, endocannabinoids may have deleterious effects under some circumstances. Irrespective of these points, however, it now appears clear that the endocannabinoid system functions within the CNS in vivo, where it may have complex and biologically significant effects.