ArticleFrontiers in behavioral neuroscience2017
Persistent Decreases in Adult Subventricular and Hippocampal Neurogenesis Following Adolescent Intermittent Ethanol Exposure.
Article in Frontiers in behavioral neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Adolescent Ethanol Exposure Disrupts the Mature Phenotype of Surviving Neuroprogenitors in Female Mice.Hippocampus · 2026Article
- Neurotoxic biomarkers of ethanol exposure: from adolescent vulnerability to adult voluntary intake in rats of both sexes.The international journal of neuropsychopharmacology · 2025Article
- Article
- Effects of adolescent alcohol exposure on oligodendrocyte lineage cells and myelination in mice: Age and subregion differences.IBRO neuroscience reports · 2024Article
- Light Alcohol Consumption Promotes Early Neurogenesis Following Ischemic Stroke in Adult C57BL/6J Mice.Biomedicines · 2023Article
- Serotonergic mediation of the brain-wide neurogenesis: Region-dependent and receptor-type specific roles on neurogenic cellular transformation.Current research in neurobiology · 2023Review
- The Influence of Sex on Hippocampal Neurogenesis and Neurotrophic Responses on the Persistent Effects of Adolescent Intermittent Ethanol Exposure into Adulthood.Neuroscience · 2022Article
- Impact of adolescent intermittent ethanol exposure on interneurons and their surrounding perineuronal nets in adulthood.Alcoholism, clinical and experimental research · 2022Article
- Cholinergic and Neuroimmune Signaling Interact to Impact Adult Hippocampal Neurogenesis and Alcohol Pathology Across Development.Frontiers in pharmacology · 2022Review
- Areas of Convergence and Divergence in Adolescent Social Isolation and Binge Drinking: A Review.Frontiers in behavioral neuroscience · 2022Review
- Primed for addiction: A critical review of the role of microglia in the neurodevelopmental consequences of adolescent alcohol drinking.Alcoholism, clinical and experimental research · 2021Review
- Hippocampal TNF-death receptors, caspase cell death cascades, and IL-8 in alcohol use disorder.Molecular psychiatry · 2021Article
- Functional Activation of Newborn Neurons Following Alcohol-Induced Reactive Neurogenesis.Brain sciences · 2021Article
- Consequences of adolescent alcohol use on adult hippocampal neurogenesis and hippocampal integrity.International review of neurobiology · 2021Review
- Expression of Oligodendrocyte and Oligoprogenitor Cell Proteins in Frontal Cortical White and Gray Matter: Impact of Adolescent Development and Ethanol Exposure.Frontiers in pharmacology · 2021Article
- Effect of alcohol use on the adolescent brain and behavior.Pharmacology, biochemistry, and behavior · 2020Review
- Neuroimmune and epigenetic mechanisms underlying persistent loss of hippocampal neurogenesis following adolescent intermittent ethanol exposure.Current opinion in pharmacology · 2020Review
- Dentate Gyrus Proliferative Responses After Traumatic Brain Injury and Binge Alcohol in Adult Rats.Neuroscience insights · 2020Article
- Changes in Neuroimmune and Neuronal Death Markers after Adolescent Alcohol Exposure in Rats are Reversed by Donepezil.Scientific reports · 2019Article
- Subventricular zone neural precursor cell responses after traumatic brain injury and binge alcohol in male rats.Journal of neuroscience research · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neurogenesis in hippocampal dentate gyrus (DG) and subventricular zone (SVZ) matures during adolescence to adult levels. Binge drinking is prevalent in adolescent humans, and could alter brain neurogenesis and maturation in a manner that persists into adulthood. To determine the impact of adolescent binge drinking on adult neurogenesis, Wistar rats received adolescent intermittent ethanol (AIE) exposure (5.0 g/kg/day, i.g., 2 days on/2 days off from postnatal day, P25-P54) and sacrificed on P57 or P95. Neural progenitor cell proliferation, differentiation, survival and maturation using immunohistochemistry was determined in the DG and SVZ. We found that AIE exposure decreased neurogenesis in both brain regions in adulthood (P95). In the DG at P57, AIE exposure resulted in a significant reduction of SOX2+, Tbr2+, Prox1+ and parvalbumin (PV)+IR expression, and at P95 decreased DCX+ and PV+IR expression. AIE exposure also reduced the expression of two cell proliferation markers (Ki67+ and BrdU+IR with 300 mg/kg, 2 h) at P95. The immune signaling molecule β-2 microglobulin+ and the cell death marker activated caspase-3+IR were significantly increased in the DG by AIE exposure. In the SVZ, AIE exposure decreased SOX2+, Mash1+, DCX+ and Dlx2+IR expression at P95, but not at P57. Thus, in adulthood both brain regions have reduced neurogenesis following AIE exposure. To assess progenitor cell survival and maturation, rats were treated with BrdU (150 mg/kg/day, 14 days) to label proliferating cells and were sacrificed weeks later on P95. In the hippocampus DG, AIE exposure increased survival BrdU+ cells which differentiated into Iba1+ microglia. In contrast, SVZ had decreased BrdU+ cells similar to decreased DCX+ neurogenesis. These data indicate that AIE exposure causes a lasting decrease in both adult hippocampal DG and forebrain SVZ neurogenesis with brain regional differences in the AIE response that persist into adulthood.
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