Abstract: The present invention is directed to a method of protecting cells of the nervous system from glutamate-induced cytotoxicity , such as the type that is mimicked by administration of N-methyl-D-aspartate (NMDA), and which is associated with conditions such as ischemia or glaucoma. In general, the method comprises increasing the activity of a cannabinoid agonist that binds specifically to an endogenous cannabinoid receptor, such as the endogenous cannabinoid receptors CB1 or CB2, to protect the cells against glutamate-induced neurotoxicity. This can be done either by the administration of a cannabinoid agonist such as a physiologically acceptable salt of R(+)-[2,3-dihydro-5-methyl3-[(morpholinyl)methyl]pyrrolo [1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl) methanone, preferably the mesylate salt, or by blocking degradation of naturally-occurring endogenous cannabinoid agonists in the cells, such as by inhibition of anandamide amidohydrolase.