Behavioral Neuroadaptation to Alcohol: From Glucocorticoids to Histone Acetylation.
paper
Cited
Public
- Authors
- Mons, Nicole; Beracochea, Daniel
- Year
- 2016
- Journal
- Frontiers in psychiatry
- PMID
- 27766083
- DOI
- 10.3389/fpsyt.2016.00165
- PMCID
- PMC5052254
A prime mechanism that contributes to the development and maintenance of alcoholism is the dysregulation of the hypothalamic-pituitary-adrenal axis activity and the release of glucocorticoids (cortisol in humans and primates, corticosterone in rodents) from the adrenal glands. In the brain, sustained, local elevation of glucocorticoid concentration even long after cessation of chronic alcohol consumption compromises functional integrity of a circuit, including the prefrontal cortex (PFC), the hippocampus (HPC), and the amygdala (AMG). These structures are implicated in learning and memory processes as well as in orchestrating neuroadaptive responses to stress and anxiety responses. Thus, potentiation of anxiety-related neuroadaptation by alcohol is characterized by an abnormally AMG hyperactivity coupled with a hypofunction of the PFC and the HPC. This review describes research on molecular and epigenetic mechanisms by which alcohol causes distinct region-specific adaptive changes in gene expression patterns and ultimately leads to a variety of cognitive and behavioral impairments on prefrontal- and hippocampal-based tasks. Alcohol-induced neuroadaptations involve the dysregulation of numerous signaling cascades, leading to long-term changes in transcriptional profiles of genes, through the actions of transcription factors such as [cAMP response element-binding protein (CREB)] and chromatin remodeling due to posttranslational modifications of histone proteins. We describe the role of prefrontal-HPC-AMG circuit in mediating the effects of acute and chronic alcohol on learning and memory, and region-specific molecular and epigenetic mechanisms involved in this process. This review first discusses the importance of brain region-specific dysregulation of glucocorticoid concentration in the development of alcohol dependence and describes how persistently increased glucocorticoid levels in PFC may be involved in mediating working memory impairments and neuroadaptive changes during withdrawal from chronic alcohol intake. It then highlights the role of cAMP-PKA-CREB signaling cascade and histone acetylation within the PFC and limbic structures in alcohol-induced anxiety and behavioral impairments, and how an understanding of functional alterations of these pathways might lead to better treatments for neuropsychiatric disorders.
Endocrine and molecular events that are associated with long-lasting prefrontal cortex (PFC)-based working memory impairment during withdrawal from prolonged ethanol consumption. (Left) in C57BL/6 mice, chronic ethanol consumption (6 months) followed by a 6-week withdrawal period causes excessive peak corticosterone (CORT) response, specifically in the PFC that lasts for several weeks. Protracted withdrawal also produces long-lasting deficits in pCREB and histone H4 acetylation levels in the PFC along with enduring working memory impairments. (Red) pharmacological glucocorticoid blockade in the PFC through bilateral infusion of drugs that diminish corticosteroid receptors [mineralocorticoid (spironolactone; MR) or glucocorticoid (mifepristone; GR)] activity as well as pharmacological elevation of cAMP–PKA-mediated signaling cascade through bilateral infusion of the cAMP analog Sp-cAMPS into the PFC fully prevent long-lasting alcohol-related endocrine, molecular, and behavioral changes. Adapted from Ref. (31, 47).
LLM interpretation
This figure is a conceptual diagram illustrating the endocrine, molecular, and behavioral effects of ethanol withdrawal in the prefrontal cortex (PFC) of mice. The left panel shows that withdrawal leads to increased CORT-PFC, decreased pCREB-PFC and acetyl Histone H4-PFC, blocked gene transcription, and impaired working memory (indicated by red arrows). The right panel demonstrates that pharmacological blockade of MRs/GRs or the use of cAMP analogs reverses these effects, resulting in decreased CORT-PFC, increased pCREB and acetyl Histone H4, allowed gene transcription, and improved working memory (indicated by blue arrows).
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In this knowledge base
| Title | Year | PMID |
|---|---|---|
| The genetic epidemiology of substance use disorder: A review. | 2017 | 28938182 |
External
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| Changes in neurobiological markers of reactivity to alcohol-related stimuli in alcohol-dependent patients after two years of treatment. | Rubio G et al. | — | 2025 | → |
| Decreased voluntary alcohol intake and ventral striatal epigenetic and transcriptional remodeling in male Acss2 KO mice. | Egervari G et al. | — | 2025 | → |
| Role of the Transcription Factor CREB in Ethanol-Induced Endoplasmic Reticulum Stress and Apoptosis in PC12 Cells. | Németh M et al. | — | 2025 | → |
| Altered Epigenetic Marks and Gene Expression in Fetal Brain, and Postnatal Behavioural Disorders, Following Prenatal Exposure of <i>Ogg1</i> Knockout Mice to Saline or Ethanol. | Bhatia S et al. | — | 2023 | → |
| Preventive Effects of Baclofen but Not Diazepam on Hippocampal Memory and Glucocorticoid Alterations After Prolonged Alcohol Withdrawal in Mice. | Nadia H et al. | — | 2022 | → |
| Neuroadaptability and Habit: Modern Medicine and Ayurveda. | Wallace RK et al. | — | 2021 | → |
| Roles of corticotropin-releasing factor signaling in the lateral habenula in anxiety-like and alcohol drinking behaviors in male rats. | Zuo W et al. | — | 2021 | → |
| Synaptic Plasticity and its Modulation by Alcohol. | Avchalumov Y et al. | — | 2020 | → |
| Baclofen but Not Diazepam Alleviates Alcohol-Seeking Behavior and Hypothalamic-Pituitary-Adrenal Axis Dysfunction in Stressed Withdrawn Mice. | Rabat Y et al. | — | 2019 | → |
| Targeting the Glucocorticoid Receptors During Alcohol Withdrawal to Reduce Protracted Neurocognitive Disorders. | Béracochéa D et al. | — | 2019 | → |
| Repeated diazepam administration reversed working memory impairments and glucocorticoid alterations in the prefrontal cortex after short but not long alcohol-withdrawal periods. | Dominguez G et al. | — | 2018 | → |
| Long-Term Effects of Intermittent Adolescent Alcohol Exposure in Male and Female Rats. | Marco EM et al. | — | 2017 | → |
| The genetic epidemiology of substance use disorder: A review. | Prom-Wormley EC et al. | — | 2017 | → |