ArticleAlcohol (Fayetteville, N.Y.)2015
Withdrawal from chronic intermittent alcohol exposure increases dendritic spine density in the lateral orbitofrontal cortex of mice.
Article in Alcohol (Fayetteville, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- Effect of chronic sleep restriction on ethanol preference and cortical structural plasticity.Neurobiology of sleep and circadian rhythms · 2025Article
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- Alcohol, flexible behavior, and the prefrontal cortex: Functional changes underlying impaired cognitive flexibility.Neuropharmacology · 2024Review
- Adaptations in glutathione-based redox protein signaling pathways and alcohol drinking across species.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- The Small G-Protein Rac1 in the Dorsomedial Striatum Promotes Alcohol-Dependent Structural Plasticity and Goal-Directed Learning in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Involvement of cortical input to the rostromedial tegmental nucleus in aversion to foot shock.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Article
- Chronic Intermittent Ethanol Administration during Adolescence Produces Sex Dependent Impairments in Behavioral Flexibility and Survivability.Brain sciences · 2022Article
- Orbitofrontal cortex subregion inhibition during binge-like and aversion-resistant alcohol drinking.Alcohol (Fayetteville, N.Y.) · 2022Article
- Areas of Convergence and Divergence in Adolescent Social Isolation and Binge Drinking: A Review.Frontiers in behavioral neuroscience · 2022Review
- Chronic intermittent ethanol during adolescence and adulthood alters dendritic spines in the primary motor and visual cortex in rats.Alcohol (Fayetteville, N.Y.) · 2021Article
- Adolescent Ethanol Exposure Alters Cholinergic Function and Apical Dendritic Branching Within the Orbital Frontal Cortex.Neuroscience · 2021Article
- Call for a more balanced approach to understanding orbital frontal cortex function.Behavioral neuroscience · 2021Article
- Interaction of chronic intermittent ethanol and repeated stress on structural and functional plasticity in the mouse medial prefrontal cortex.Neuropharmacology · 2021Article
- Optogenetically-induced long term depression in the rat orbitofrontal cortex ameliorates stress-induced reversal learning impairment.Neurobiology of stress · 2020Article
- Review of Orbitofrontal Cortex in Alcohol Dependence: A Disrupted Cognitive Map?Alcoholism, clinical and experimental research · 2020Review
- Selective impact of lateral orbitofrontal cortex inactivation on reinstatement of alcohol seeking in male Long-Evans rats.Neuropharmacology · 2020Article
- Article
- Comorbid HIV infection and alcohol use disorders: Converging glutamatergic and dopaminergic mechanisms underlying neurocognitive dysfunction.Brain research · 2019Review
- Article
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Authors and funding
5 authors.
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Abstract
Alcohol use disorders (AUDs) are associated with functional and morphological changes in subfields of the prefrontal cortex. Clinical and preclinical evidence indicates that the orbitofrontal cortex (OFC) is critical for controlling impulsive behaviors, representing the value of a predicted outcome, and reversing learned associations. Individuals with AUDs often demonstrate deficits in OFC-dependent tasks, and rodent models of alcohol exposure show that OFC-dependent behaviors are impaired by chronic alcohol exposure. To explore the mechanisms that underlie these impairments, we examined dendritic spine density and morphology, and NMDA-type glutamate receptor expression in the lateral OFC of C57BL/6J mice following chronic intermittent ethanol (CIE) exposure. Western blot analysis demonstrated that NMDA receptors were not altered immediately following CIE exposure or after 7 days of withdrawal. Morphological analysis of basal dendrites of layer II/III pyramidal neurons revealed that dendritic spine density was also not affected immediately after CIE exposure. However, the total density of dendritic spines was significantly increased after a 7-day withdrawal from CIE exposure. The effect of withdrawal on spine density was mediated by an increase in the density of long, thin spines with no change in either stubby or mushroom spines. These data suggest that morphological neuroadaptations in lateral OFC neurons develop during alcohol withdrawal and occur in the absence of changes in the expression of NMDA-type glutamate receptors. The enhanced spine density that follows alcohol withdrawal may contribute to the impairments in OFC-dependent behaviors observed in CIE-treated mice.
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Registered trials
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