ArticlePloS one2013
Novel oxytocin gene expression in the hindbrain is induced by alcohol exposure: transgenic zebrafish enable visualization of sensitive neurons.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Enteroendocrine cells wire the gut-brain vagal axis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Melanin-Concentrating Hormone (MCH): Role in Mediating Reward-Motivated and Emotional Behavior and the Behavioral Disturbances Produced by Repeated Exposure to Reward Substances.International journal of molecular sciences · 2025Review
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- Subpopulations of hypocretin/orexin neurons differ in measures of their cell proliferation, dynorphin co-expression, projections, and response to embryonic ethanol exposure.Scientific reports · 2023Article
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- Protective effects of resveratrol on the ethanol-induced disruption of retinogenesis in pluripotent stem cell-derived organoids.FEBS open bio · 2023Article
- Embryonic ethanol exposure induces ectopic Hcrt and MCH neurons outside hypothalamus in rats and zebrafish: Role in ethanol-induced behavioural disturbances.Addiction biology · 2022Article
- Social isolation modulates appetite and avoidance behavior via a common oxytocinergic circuit in larval zebrafish.Nature communications · 2022Article
- Reproductive roles of the vasopressin/oxytocin neuropeptide family in teleost fishes.Frontiers in endocrinology · 2022Review
- Alcohol and oxytocin: Scrutinizing the relationship.Neuroscience and biobehavioral reviews · 2021Review
- Article
- Modeling alcohol-induced neurotoxicity using human induced pluripotent stem cell-derived three-dimensional cerebral organoids.Translational psychiatry · 2020Article
- Zebrafish Shoaling, Its Behavioral and Neurobiological Mechanisms, and Its Alteration by Embryonic Alcohol Exposure: A Review.Frontiers in behavioral neuroscience · 2020Review
- Zebrafish oxytocin neurons drive nocifensive behavior via brainstem premotor targets.Nature neuroscience · 2019Article
- Diving into the world of alcohol teratogenesis: a review of zebrafish models of fetal alcohol spectrum disorder.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2018Review
- Article
- Comparison of molecular marker expression in early zebrafish brain development following chronic ethanol or morpholino treatment.Experimental brain research · 2017Article
- Zebrafish Models of Prader-Willi Syndrome: Fast Track to Pharmacotherapeutics.Diseases (Basel, Switzerland) · 2016Article
- Whole-brain activity mapping onto a zebrafish brain atlas.Nature methods · 2015Article
- Zebrafish models in translational research: tipping the scales toward advancements in human health.Disease models & mechanisms · 2014Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundFetal Alcohol Spectrum Disorders (FASD) are a collection of disorders resulting from fetal ethanol exposure, which causes a wide range of physical, neurological and behavioral deficits including heightened susceptibility for alcoholism and addictive disorders. While a number of mechanisms have been proposed for how ethanol exposure disrupts brain development, with selective groups of neurons undergoing reduced proliferation, dysfunction and death, the induction of a new neurotransmitter phenotype by ethanol exposure has not yet been reported. PRINCIPAL
findingsThe effects of embryonic and larval ethanol exposure on brain development were visually monitored using transgenic zebrafish expressing cell-specific green fluorescent protein (GFP) marker genes. Specific subsets of GFP-expressing neurons were highly sensitive to ethanol exposure, but only during defined developmental windows. In the med12 mutant, which affects the Mediator co-activator complex component Med12, exposure to lower concentrations of ethanol was sufficient to reduce GFP expression in transgenic embryos. In transgenic embryos and larva containing GFP driven by an oxytocin-like (oxtl) promoter, ethanol exposure dramatically up-regulated GFP expression in a small group of hindbrain neurons, while having no effect on expression in the neuroendocrine preoptic area.
conclusionsAlcohol exposure during limited embryonic periods impedes the development of specific, identifiable groups of neurons, and the med12 mutation sensitizes these neurons to the deleterious effects of ethanol. In contrast, ethanol exposure induces oxtl expression in the hindbrain, a finding with profound implications for understanding alcoholism and other addictive disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.