Journal
BIOLOGICAL PSYCHIATRY
Volume 66, Issue 1, Pages 9-16Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2008.10.047
Keywords
Amygdala; endocannabinoids; fMRI; genetics; individual differences; reward; threat; ventral striatum
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Funding
- National institutes of Health (NIH) [HL040962, MH072837]
- National Alliance for Research on Schizophrenia and Depression (NARSAD)
- National Institute on Alcohol Abuse and Alcoholism (NIAAA)
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Background: Fatty acid amide hydrolase (FAAH) is a key enzyme in regulating endocannabinoid (eCB) signaling. A common single nucleotide polymorphism (C385A) in the human FAAH gene has been associated with increased risk for addiction and obesity. Methods: Using imaging genetics in 82 healthy adult volunteers, we examined the effects of FAAH C385A on threat- and reward-related human brain function. Results: Carriers of FAAH 385A, associated with reduced enzyme and possibly increased eCB signaling, had decreased threat-related amygdala reactivity but increased reward-related ventral striatal reactivity in comparison with C385 homozygotes. Similarly divergent effects of FAAH C385A genotype were manifest at the level of brain-behavior relationships. The 385A carriers showed decreased correlation between amygdala reactivity and trait anxiety but increased correlation between ventral striatal reactivity and delay discounting, an index of impulsivity. Conclusions: Our results parallel pharmacologic and genetic dissection of eCB signaling, are consistent with the psychotropic effects of Delta(9)-tetrahydrocannabinol, and highlight specific neural mechanisms through which variability in eCB signaling impacts complex behavioral processes related to risk for addiction and obesity.
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