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. 2015 Nov 18;41(6):1598–1609. doi: 10.1038/npp.2015.318

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Copyright © 2016 American College of Neuropsychopharmacology

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Fluoxetine augments amygdala anandamide levels and inhibits fatty acid amide hydrolase (FAAH) activity. Chronic fluoxetine treatment increased basolateral amygdala (BLA) levels of anandamide (a) and oleoylethanolamide (b). Anandamide levels were increased in the dorsal hippocampus (HC) and dorsal striatum, but not prefrontal cortex (PFC), after chronic fluoxetine (c). Chronic fluoxetine increased 2-arachidonylglycerol (2-AG) levels in the dorsal hippocampus but not in the other brain regions examined (d). BLA expression of a suite of genes involved in endocannabinoid (eCB) synthesis and degradation was normal after chronic fluoxetine (e). FAAH activity in the BLA was reduced after chronic fluoxetine (f). Data are means±SEM. *P<0.05. Flx, fluoxetine; Wtr, water.