exchanger in mitochondria (mNCX) to regulate intracellular calcium levels, an important determinant of neuronal survival. After treatment with an inhibitor of mNCX (CGP-37157), no detectable neuroprotection from ethanol toxicity was observed for either CBD or KLS-13019. Furthermore, AM630 (CB2 antagonist) significantly attenuated CBD-mediated neuroprotection, while having no detectable effect on neuroprotection from KLS-13019. Our studies indicated KLS-13019 was more potent and less toxic than CBD. Both compounds can act through mNCX. KLS-13019 may provide an alternative to CBD as a therapeutic candidate to treat diseases associated with oxidative stress.

KEYWORDS:

Cannabidiol; Cannabis; Ethanol; Hippocampal cultures; Mitochondrial Na

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