FAAH genetic variation enhances fronto-amygdala function in mouse and human
Open accessAbstract
Cross-species studies enable rapid translational discovery and produce the broadest impact when both mechanism and phenotype are consistent across organisms. We developed a knock-in mouse that biologically recapitulates a common human mutation in the gene for fatty acid amide hydrolase (FAAH) (C385A; rs324420), the primary catabolic enzyme for the endocannabinoid anandamide. This common polymorphism impacts the expression and activity of FAAH, thereby increasing anandamide levels. Here, we show that the genetic knock-in mouse and human variant allele carriers exhibit parallel alterations in biochemisty, neurocircuitry and behaviour. Specifically, there is reduced FAAH expression associated with the variant allele that selectively enhances fronto-amygdala connectivity and fear extinction learning, and decreases anxiety-like behaviours. These results suggest a gain of function in fear regulation and may indicate for whom and for what anxiety symptoms FAAH inhibitors or exposure-based therapies will be most efficacious, bridging an important translational gap between the mouse and human. Fatty acid amide hydrolase (FAAH) is a key regulator of endocannabinoid signalling. Here, the authors develop a knock-in mouse that recapitulates a common human mutation in the FAAH gene and demonstrate parallel neural and behavioural alterations across species, suggesting a gain-of-function in fear regulation.
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A genetic knock-in mouse recapitulating human FAAH mutation C385A presented reduced FAAH expression associated with the variant allele that selectively enhanced fronto-amygdala connectivity and fear extinction learning and decreased anxiety-like behaviours, suggesting a possible molecular genetic target.
“From the perspective of the preoccupation/anticipation stage, a genetic knock-in mouse that bio logically recapitulates a common human mutation in the gene for fatty acid amide hydrolase (C385A [Pro129Thr], rs324420) presented a reduction of fatty acid amide hydrolase expression associated with the variant allele that selectively enhanced fronto-amygdala connectivity and fear extinction learning”
From Neurobiology of addiction: a neurocircuitry analysis (2016) · cites this paper as [165]
The 385A allele (rs324420) is associated with reduced indices of trait anxiety, enhanced corticoamygdala connectivity, and reduced activation and accelerated habituation of amygdala BOLD responses to threat cues.
“This polymorphism (385A allele; rs324420) has been repeatedly associated with reduced indices of trait anxiety, as well as enhanced corticoamygdala connectivity and reduced activation and accelerated habituation of amygdala blood-oxygen-level dependent (BOLD) responses to threat cues (Demers et al., 2016; Dincheva et al., 2015; Gee et al., 2016; Gunduz-Cinar et al., 2013b; Hariri et al., 2009).”
From The endocannabinoid system as a target for novel anxiolytic drugs (2017) · cites this paper as Dincheva et al., 2015
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Self-citation
- Authors
- Dincheva, I., Drysdale, A. T., Hartley, C. A., Johnson, D. C., Jing, D., King, E. C., Ra, S., Gray, J. M., Yang, R., DeGruccio, A. M., Huang, C., Cravatt, B. F., Glatt, C. E., Hill, M. N., Casey, B. J., & Lee, F. S.
- Affiliations
- Cornell University (US)
- University of Calgary (CA)
- Ingenious Targeting Laboratory (United States) (US)
- Scripps Research Institute (US)
- Corresponding author
- Casey, B. J.
- Lee, Francis S.
- ORCID
- Venue
- Nature Communications
- Published
- 2015-03-03
- Volume
- 6
- Issue
- 1
- Pages
- 6395-6395
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4351757
- OpenAlex
- W2003159048
- Cited by
- 289
- References
- 56
- Citations by year
- 2026: 11 · 2025: 21 · 2024: 25 · 2023: 28 · 2022: 28 · 2021: 34 · 2020: 29 · 2019: 24 · 2018: 18 · 2017: 27 · 2016: 18 · 2015: 26
- FWCI
- 21.37
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- New York Community Trust
- National Institutes of Health (MH079513, DA017259)
- Weill Cornell Medical College
- Cumming School of Medicine, University of Calgary
- Canadian Institutes of Health Research
- National Institute of Mental Health (P50MH079513, MH079513, R25MH060478, MH060478)
- National Institute on Drug Abuse (DA-017259, P01DA017259)
- National Eye Institute (EY007138, T32EY007138)
- National Institute of General Medical Sciences (GM 07739, T32GM007739)
- National Institute of Neurological Disorders and Stroke (NS052819, R01NS052819)
- Topics
- Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- fatty acid amide hydrolase, anandamide, endocannabinoid system, knock-in mice, fear extinction learning, anxiety-like behavior, fear regulation, FAAH inhibitors, translational research
- MeSH terms
- Fatty Acid Amide Hydrolases, Amidohydrolases, Amygdala, Animals, Extinction, Psychological, Fear, Frontal Lobe, Humans, Image Processing, Computer-Assisted, Immunohistochemistry, Magnetic Resonance Imaging, Species Specificity, Mass Spectrometry, Blotting, Western, Gene Expression Regulation, Enzymologic, Polymorphism, Single Nucleotide, Mice, Gene Knock-In Techniques
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