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. 2018 May 14;15:142. doi: 10.1186/s12974-018-1166-9

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© The Author(s). 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 8 — CPD-4645 rescues BBB integrity via endocannabinoid dependent and independent mechanisms. Blockade of endocannabinoid signaling with rimonabant and AM630 (3 mg/kg) does not reverse the BBB protective effects of MAGL inhibition in the inflammation-driven LPS model (a), whereas blockade of endocannabinoid signaling partially reverses the protective effects of MAGL inhibition (administered 30 min post lesion) in the photothrombotic ischemia-driven model (b) as measured by extravasation of 70 kDa FITC-dextran into the brain parenchyma. Data were plotted with means ± SEM (n = 6–9 mice/group) and analyzed with one-way ANOVA with Bonferroni’s post-hoc test. Significance is shown as *p ≤ 0.05, **p ≤ 0.01