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The Journal of Neuroscience, November 15, 2002, 22(22):9771-9775

Increased Severity of Stroke in CB1 Cannabinoid Receptor Knock-Out Mice

Sophie Parmentier-Batteur¹, Kunlin Jin¹, Xiao Ou Mao¹, Lin Xie¹, and David A. Greenberg^{1, 2}

¹ Buck Institute for Age Research, Novato, California 94945, and ² Department of Neurology, University of California, San Francisco, California 94143

Endogenous cannabinoid signaling pathways have been implicated in protection of the brain from hypoxia, ischemia, and trauma, but the mechanism for these protective effects is uncertain. We found that in CB1 cannabinoid receptor knock-out mice, mortality from permanent focal cerebral ischemia was increased, infarct size and neurological deficits after transient focal cerebral ischemia were more severe, cerebral blood flow in the ischemic penumbra during reperfusion was reduced, and NMDA neurotoxicity was increased compared with wild-type littermates. These findings indicate that endogenous cannabinoid signaling pathways protect mice from ischemic stroke by a mechanism that involves CB1 receptors, and suggest that both blood vessels and neurons may be targets of this protective effect.

Key words: ischemia; cannabinoid; CB1 receptor; stroke; cerebral blood flow; NMDA

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22229771-05$05.00/0

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