ArticleFrontiers in neuroscience2015
Binge ethanol exposure during adolescence leads to a persistent loss of neurogenesis in the dorsal and ventral hippocampus that is associated with impaired adult cognitive functioning.
Article in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 2 of them syntheses that pooled it.
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Who cites it
105 citing papers in PubMed, 2 syntheses or guidelines pooled it, 162 citations in OpenAlex.
- Impact of Omega-3 Polyunsaturated Fatty Acids on Alcohol Use and Negative Consequences: A Systematic Review.Nutrition reviews · 2025Pooled it
- Age-related differences in the effect of chronic alcohol on cognition and the brain: a systematic review.Translational psychiatry · 2022Pooled it
- Adolescent Ethanol Exposure Disrupts the Mature Phenotype of Surviving Neuroprogenitors in Female Mice.Hippocampus · 2026Article
- Super-resolved, three-dimensional spatial transcriptomics reveals cell-type and brain-region-specific modulation of key epitranscriptomic switches following adolescent alcohol exposure.bioRxiv : the preprint server for biology · 2026Article
- Adolescent adversity persistently induces proinflammatory HMGB1 signaling and disrupts the basal forebrain cholinergic system in female rats.Neurobiology of stress · 2026Article
- Mechanisms of Alcohol Interference with Hippocampal Neurogenesis and its Repair Strategies.Molecular neurobiology · 2025Review
- Neurotoxic biomarkers of ethanol exposure: from adolescent vulnerability to adult voluntary intake in rats of both sexes.The international journal of neuropsychopharmacology · 2025Article
- Chrysophanol Attenuates Cognitive Impairment, Neuroinflammation, and Oxidative Stress by TLR4/ NFκB-Nrf2/HO-1 Signaling in Ethanol-Induced Neurodegeneration.Neurochemical research · 2025Article
- Article
- Adolescent alcohol exposure disrupts episodic-like memory by impairing dopamine synapses in the mouse prelimbic cortex.Neuropharmacology · 2025Article
- Impact of Neuroimmune System Activation by Adolescent Binge Alcohol Exposure on Adult Neurobiology.Advances in experimental medicine and biology · 2025Review
- Adolescent Alcohol and the Spectrum of Cognitive Dysfunction in Aging.Advances in experimental medicine and biology · 2025Review
- Adolescent binge alcohol exposure accelerates Alzheimer's disease-associated basal forebrain neuropathology through proinflammatory HMGB1 signaling.Frontiers in aging neuroscience · 2025Article
- A neural circuit for alcohol withdrawal-induced hyperalgesia in a nondependent state.Science advances · 2024Article
- Ethanol Exacerbates the Alzheimer's Disease Pathology in the 5xFAD Mouse Model.Neuroglia (Basel, Switzerland) · 2024Article
- Adolescent intermittent ethanol (AIE) sensitized fever in male Sprague Dawley rats exposed to poly I:C in adulthood.Brain, behavior, and immunity · 2024Article
- Ethanol changes Nestin-promoter induced neural stem cells to disturb newborn dendritic spine remodeling in the hippocampus of mice.Neural regeneration research · 2024Article
- Epigenetic regulation of microglia and neurons by proinflammatory signaling following adolescent intermittent ethanol (AIE) exposure and in human AUD.Advances in drug and alcohol research · 2024Review
- Exercise leads to sex-specific recovery of behavior and pathological AD markers following adolescent ethanol exposure in the TgF344-AD model.Frontiers in behavioral neuroscience · 2024Article
- HMGB1 neuroimmune signaling and REST-G9a gene repression contribute to ethanol-induced reversible suppression of the cholinergic neuron phenotype.Molecular psychiatry · 2023Article
45 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
Funding
Abstract
Adolescence is a developmental period that coincides with the maturation of adult cognitive faculties. Binge drinking is common during adolescence and can impact brain maturation. Using a rodent model of adolescent intermittent ethanol (AIE; 5.0 g/kg, i.g., 20% EtOH w/v; 2 days on/2 days off from postnatal day [P]25 to P55), we discovered that AIE treatment reduced neurogenesis (i.e., doublecortin-immunoreactive [DCX + IR] cells) in both the dorsal and ventral hippocampal dentate gyrus of late adolescent (P56) male Wistar rats that persisted during abstinence into adulthood (P220). This reduction in neurogenesis was accompanied by a concomitant reduction in proliferating cells (Ki-67) and an increase in cell death (cleaved caspase-3). In the hippocampus, AIE treatment induced a long-term upregulation of neuroimmune genes, including Toll-like receptor 4 (TLR4) and its endogenous agonist high-mobility group box 1 as well as several proinflammatory signaling molecules. Administration of lipopolysaccharide, a gram-negative endotoxin agonist at TLR4, to young adult rats (P70) produced a similar reduction of DCX + IR cells that was observed in AIE-treated animals. Behaviorally, AIE treatment impaired object recognition on the novel object recognition task when assessed from P163 to P165. Interestingly, object recognition memory was positively correlated with DCX + IR in both the dorsal and ventral hippocampal dentate gyrus while latency to enter the center of the apparatus was negatively correlated with DCX + IR in the ventral dentate gyrus. Together, these data reveal that adolescent binge ethanol exposure persistently inhibits neurogenesis throughout the hippocampus, possibly through neuroimmune mechanisms, which might contribute to altered adult cognitive and emotive function.
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