The human costs of stroke are very large and growing; it is the third largest cause of death in the United States and survivors are often faced with loss of ability to function independently. There is a large need for therapeutic approaches that act to protect neurons from the injury produced by ischemia and reperfusion. The goal of this review is to introduce and discuss the available data that endogenous cannabinoid signaling is altered during ischemia and that it contributes to the consequences of ischemia-induced injury. Overall, the available data suggest that inhibition of CB1 receptor activation together with increased CB2 receptor activation produces beneficial effects.
Keywords: CB1 cannabinoid receptor, CB2 cannabinoid receptor, rimonabant, fatty acid amide hydrolase, N-arachidonylethanolamine, anandamide, 2-arachidonoylglycerol
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