• Angel Arevalo-Martin, Daniel Garcia-Ovejero, and Eduardo Molina-Holgado.
• Unidad de Neurologia Experimental, Hospital Nacional de Paraplejicos (SESCAM), Toledo, Spain. aarevalom@sescam.jccm.es
• Neurobiol. Dis. 2010 May 1;38(2):304-12.

AbstractA series of pathological events secondary to spinal cord injury (SCI) contribute to the spread of the damage, which aggravates neurological deficits. Here we report that a single dose of the neuroprotective endocannabinoid 2-arachidonoyl glycerol (2-AG) administered early after SCI reduces lesion expansion, which was prevented by simultaneous blockade of both CB1 and CB2 receptors but not by blockade of either receptor alone. Treatment with 2-AG also preserves the white matter around the epicenter of the injury. Moreover, in the preserved white matter, 2-AG protects myelin from damage and reduces oligodendrocyte loss. In addition to these protective actions at the epicenter region, 2-AG also inhibits the myelin damage and delayed oligodendrocyte loss induced at 10mm from the epicenter. Interestingly, the early protective action of 2-AG is maintained 28 days after injury, when the lesion size is still smaller and the preservation of white matter is better in 2-AG-treated animals. Therefore, our results show that 2-AG protects from the expansion of the lesion and white matter damage, which suggest that this endogenous cannabinoid may be useful as a protective treatment for acute SCI.Copyright 2010 Elsevier Inc. All rights reserved.

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