Alcohol self-administration acutely stimulates the hypothalamic-pituitary-adrenal axis, but alcohol dependence leads to a dampened neuroendocrine state
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Clinical studies link disruption of the neuroendocrine stress system with alcoholism, but remaining unknown is whether functional differences in the hypothalamic‐pituitary‐adrenal (HPA) axis precede alcohol abuse and dependence or result from chronic exposure to this drug. Using an operant self‐administration animal model of alcohol dependence and serial blood sampling, we show that long‐term exposure to alcohol causes significant impairment of HPA function in adult male Wistar rats. Acute alcohol (voluntary self‐administration or experimenter‐administered) stimulated the release of corticosterone and its upstream regulator, adrenocorticotropic hormone, but chronic exposure sufficient to produce dependence led to a dampened neuroendocrine state. HPA responses to alcohol were most robust in ‘low‐responding’ non‐dependent animals (averaging < 0.2 mg/kg/session), intermediate in non‐dependent animals (averaging ∼0.4 mg/kg/session), and most blunted in dependent animals (averaging ∼1.0 mg/kg/session) following several weeks of daily 30‐min self‐administration sessions, suggesting that neuroendocrine tolerance can be initiated prior to dependence and relates to the amount of alcohol consumed. Decreased expression of corticotropin‐releasing factor (CRF) mRNA expression in the paraventricular nucleus of the hypothalamus and reduced sensitivity of the pituitary to CRF may contribute to, but do not completely explain, neuroendocrine tolerance. The present results, combined with previous studies, suggest that multiple adaptations to stress regulatory systems may be brought about by excessive drinking, including a compromised hormonal response and a sensitized brain stress response that together contribute to dependence.
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Rats made dependent using the chronic intermittent alcohol vapor model exhibit a blunted corticosterone response.
“Similar effects have been observed in animal models in which rats that are made dependent using the chronic intermittent alcohol vapor model exhibit a blunted corticosterone response (Richardson et al., 2008).”
From Drug Addiction: Hyperkatifeia/Negative Reinforcement as a Framework for Medications Development (2021) · cites this paper as Richardson et al., 2008
Binge and heavy alcohol use, high nicotine use, and other psychostimulant use reduce the increased cortisol responses observed with acute alcohol or drug intake.
“binge and heavy alcohol use, but also high nicotine and other psychostimulant use, reduces the well-known increased cortisol responses observed with acute alcohol/drug intake”
From Role of addiction and stress neurobiology on food intake and obesity (2018) · cites this paper as Richardson, Lee, O'Dell, Koob, & Rivier, 2008
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- Authors
- Richardson, H. N., Lee, S. Y., O’Dell, L. E., Koob, G. F., & Rivier, C. L.
- Affiliations
- Scripps Research Institute (US)
- Salk Institute for Biological Studies (US)
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2008-10
- Volume
- 28
- Issue
- 8
- Pages
- 1641-1653
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- PMC
- PMC2748838
- OpenAlex
- W2161039633
- Cited by
- 294
- References
- 79
- Citations by year
- 2026: 9 · 2025: 11 · 2024: 7 · 2023: 22 · 2022: 19 · 2021: 12 · 2020: 14 · 2019: 16 · 2018: 26 · 2017: 14 · 2016: 15 · 2015: 22 · 2014: 20 · 2013: 26 · 2012: 18
- FWCI
- 6.29
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- European Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (R01AA008459, AA12602, AA-06420, AA-08459, P50AA006420, R37AA008459, R01AA012602, T32AA007456, P60AA006420)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Keywords
- alcoholism, hypothalamic-pituitary-adrenal axis, alcohol self-administration, corticosterone, ACTH, corticotropin-releasing factor, paraventricular nucleus, stress response, chronic ethanol exposure
- MeSH terms
- Adrenocorticotropic Hormone, Ethanol, Alcoholism, Animals, Central Nervous System Depressants, Corticosterone, Corticotropin-Releasing Hormone, Disease Models, Animal, Dose-Response Relationship, Drug, Drug Administration Schedule, Endocrine System Diseases, Hypothalamo-Hypophyseal System, Male, Neurosecretory Systems, Paraventricular Hypothalamic Nucleus, Pituitary-Adrenal System, RNA, Messenger, Rats, Wistar, Alcohol-Induced Disorders, Nervous System, Rats
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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