Deficient endocannabinoid signaling in the central amygdala contributes to alcohol dependence-related anxiety-like behavior and excessive alcohol intake
Open accessAbstract
Negative emotional states that are associated with excessive alcohol intake, particularly anxiety-like states, have been linked to opponent processes in the central nucleus of the amygdala (CeA), affecting stress-related transmitters and monoamines. This study extends these observations to include endocannabinoid signaling in alcohol-dependent animals. Rats and mice were exposed to chronic intermittent alcohol with vapor inhalation or liquid diet to induce dependence. In vivo microdialysis was used to estimate interstitial concentrations of endocannabinoids [N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG)] and amino acids (glutamate and GABA) in rat CeA. Additionally, we evaluated the inhibition of endocannabinoids clearance enzymes [monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase] on anxiety-like behavior and alcohol consumption in alcohol-dependent rats and mice. Results revealed that alcohol dependence produced decreases in baseline 2-AG dialysate levels and increases in baseline levels of glutamate and GABA. Acute alcohol abstinence induced an enhancement of these dependence-induced effects and the levels of 2-AG and GABA were restored upon alcohol re-exposure. Additional studies showed that the increased CeA 2-AG levels induced by restraint stress and alcohol self-administration were blunted in alcohol-dependent rats. Pharmacological studies in rats and mice showed that anxiety-like behavior and alcohol consumption were increased in alcohol-dependent animals, and these behavioral effects were attenuated mainly by MAGL inhibitors [MJN110 (10 and 20 mg/kg) in rats and JZL184 (1 and 3 mg/kg) in mice]. The present results suggest a key role for endocannabinoid signaling in motivational neuroadaptations during alcohol dependence, in which a deficiency in CeA 2-AG signaling in alcohol-dependent animals is linked to stress and excessive alcohol consumption.
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For alcohol, chronic alcohol exposure increases brain 2-AG and AEA, particularly in basal forebrain areas, in rodents, but decreases in both 2-AG and AEA are observed in the CeA during withdrawal.
“For alcohol, chronic alcohol exposure increases brain 2-AG (Caillé et al., 2007;Alvarez-Jaimes et al., 2009) and N-arachidonoylethanolamine (AEA), particularly in basal forebrain areas, in rodents (González et al., 2004;Vinod et al., 2006), but decreases in both 2-AG and AEA were observed in the CeA during withdrawal (Serrano et al., 2018).”
From Drug Addiction: Hyperkatifeia/Negative Reinforcement as a Framework for Medications Development (2021) · cites this paper as Serrano et al., 2018
The Results (page unavailable) report that CeA 2-AG decreased during 12 hours of abstinence in alcohol-dependent rats. They report no effect of alcohol history or sampling time on CeA AEA levels, so the claim that AEA also decreased during withdrawal is not supported. The earlier increases elsewhere in the brain are attributed to other citations in the citing sentence. (LLM, conf=0.92)
Experimental — accuracy not yet measuredBoth FAAH inhibitors and MAGL inhibitors decrease withdrawal-induced anxiety-like behavior and decrease alcohol consumption in alcohol-dependent rats.
“Both FAAH inhibitors and MAGL inhibitors, which functionally increase endocannabinoids, decreased withdrawal-induced anxiety-like behavior and decreased alcohol consumption in alcoholdependent rats (Serrano et al., 2018).”
From Drug Addiction: Hyperkatifeia/Negative Reinforcement as a Framework for Medications Development (2021) · cites this paper as Serrano et al., 2018
The results on anxiety-like behavior report improvement with the MAGL inhibitor MJN110 in alcohol-dependent rats, and the discussion says both MAGL and FAAH inhibitors ameliorated dependence-associated anxiety-like behavior. The alcohol-intake results report a significant reduction with MJN110, but the discussion states that FAAH inhibition did not consistently alter alcohol consumption in dependent rats or mice. Thus, the claim overstates the alcohol-consumption finding for FAAH inhibitors (sections on anxiety-like behavior, FAAH inhibition, and 2-AG clearance inhibition; page unavailable). (LLM, conf=0.92)
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- Authors
- Serrano, A., Pavon, F. J., Buczynski, M. W., Schlosburg, J., Natividad, L. A., Polis, I. Y., Stouffer, D. G., Zorrilla, E. P., Roberto, M., Cravatt, B. F., Martin-Fardon, R., Rodriguez de Fonseca, F., & Parsons, L. H.
- Affiliations
- Scripps Research Institute (US)
- Virginia Commonwealth University (US)
- Corresponding author
- Serrano, Antonia
- ORCID
- Venue
- Neuropsychopharmacology
- Published
- 2018-04-05
- Volume
- 43
- Issue
- 9
- Pages
- 1840-1850
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC6046053
- OpenAlex
- W2795837921
- Cited by
- 83
- References
- 71
- Citations by year
- 2026: 7 · 2025: 13 · 2024: 4 · 2023: 9 · 2022: 12 · 2021: 17 · 2020: 9 · 2019: 10 · 2018: 2
- FWCI
- 6.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
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- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- RISalud Institutional Health Repository of Andalucía (submittedVersion, other-oa)
- Funders
- European Commission
- Ministerio de Economía y Competitividad (PI16/, PI16/01953, RD12/0028/0001)
- Ministerio de Sanidad, Servicios Sociales e Igualdad (PND2017/043)
- Junta de Andalucía (CTS-433)
- National Institutes of Health (AA017447, AA006420, 5r37aa017447-15)
- Plan Nacional sobre Drogas
- Instituto de Salud Carlos III (PI16/, CP14/00212, RD12/0028/0001, CP14/00173, CP14/00173 and CP14/00212, PI17/02026, PI16/01953)
- European Regional Development Fund (CTS-433, CP14/00173, CP14/00212)
- National Institute on Alcohol Abuse and Alcoholism (K99AA025393, R37-AA017447, R01AA020404, R01AA022249, R01AA015566, P50AA006420, R21AA024146, R01AA017447, P60AA006420)
- National Institute on Drug Abuse (R00DA035865, K99DA037344, R00DA037344)
- Topics
- Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- endocannabinoid signaling, central amygdala, alcoholism, anxiety-like behavior, excessive alcohol intake, 2-arachidonoylglycerol, anandamide, monoacylglycerol lipase, fatty acid amide hydrolase, JZL184, glutamate, GABA, alcohol self-administration, restraint stress, alcohol abstinence, neural adaptation
- MeSH terms
- Fatty Acid Amide Hydrolases, Ethanol, Alcoholism, Amidohydrolases, Animals, Anxiety, Central Nervous System Depressants, gamma-Aminobutyric Acid, Male, Mice, Inbred C57BL, Monoacylglycerol Lipases, Rats, Wistar, Glutamic Acid, Endocannabinoids, Central Amygdaloid Nucleus
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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