A neuroprotective role for DSE? Exogeneous cannabinoids are known to have a neuroprotective role; a recent
study has shown that mice in which CB1Rs had been selectively eliminated from glutamatergic principal cells
were much more subject than control mice to neurotoxic events induced by kainate (Marsicano et al., 2003; for
a review Piomelli et al., 2000). We suggest that this neuroprotective role could come from DSE by the following
mechanism: intracellular calcium increases in response to excitatory ionotropic receptor activation can trigger
excitotoxicity and neuronal death following, for example, ischemic brain injury; the accumulation of intracellular
calcium during such noxious events could lead to cannabinoid production, to CB1R activation and, finally, to a
DSE-like presynapticinhibition of glutamatergictransmission with neuroprotective effects.