Comparison of molecular marker expression in early zebrafish brain development following chronic ethanol or morpholino treatment

Zhang, Chengjin; Boa-Amponsem, Oswald; Cole, Gregory J.

doi:10.1007/s00221-017-4977-5

Cited by 4 publications

(3 citation statements)

References 53 publications

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“…In the context of mammalian blood alcohol content (BAC), a media ethanol concentration of 171–342mM corresponds to embryonic tissue BACs of 0.20–0.40 g/dL, which are levels within the biological tolerance of humans. Moreover, the ethanol exposure concentrations used in our study are within range of concentrations used in several other FASD zebrafish studies (Joya, Garcia-Algar, Vall, & Pujades, 2014; Kalueff, Stewart, & Gerlai, 2014; Pan, Kaiguo, Razak, Westwood, & Gerlai, 2011; Sylvain, Brewster, & Ali, 2011; Yin et al, 2014; Zhang, Boa-Amponsem, & Cole, 2017; Zhang et al, 2014; Zhang, Ojiaku, & Cole, 2013).…”

Section: Methodsmentioning

confidence: 55%

Differentially sensitive neuronal subpopulations in the central nervous system and the formation of hindbrain heterotopias in ethanol‐exposed zebrafish

Buckley

Sidik

Kar

et al. 2019

Birth Defects Research

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Background A cardinal feature of prenatal ethanol exposure is CNS damage, resulting in a continuum of neurological and behavioral impairments that are described by the term Fetal Alcohol Spectrum Disorders (FASD). FASDs are variable and depend on several factors, including the amount, timing and duration of prenatal ethanol exposure. To enhance interventions for CNS dysfunction, it is necessary to identify ethanol-sensitive neuronal populations and expand the understanding of factors that modify ethanol teratogenesis. Methods: To investigate the susceptibility of different neuronal subtypes, we exposed transgenic zebrafish (Danio rerio) to several ethanol concentrations (0.25%, 0.5%, 1.0%, 1.5% or 2.0%), at different hours post fertilization (hpf) (0 hpf, 6 hpf or 24 hpf), for various durations (0–24hpf, 0–48hpf, 4–24hpf, 6–24hpf, 6–48hpf or 24–48hpf). Following exposure, embryo survival rates were determined, and CNS neurogenesis, differentiation and patterning was assessed. Results: Embryo survival rates decrease as ethanol concentrations increase and drastically decline when exposed from 0–24hpf compared to 4–24hpf. Abnormal tangential migration of facial motor neurons is observed in isl1:gfp embryos exposed to ethanol concentrations as low as 0.25%, and the formation of IVth ventricle heterotopias are revealed by embryos exposed to ≥1.0% ethanol. Whereas, expression of olig2:dsred and ptf1a:gfp in the cerebellum and spinal cord are largely unaffected. While levels of etv4 mRNA are overtly resistant to ethanol, we observe significant reductions in ptch2 mRNA levels. Conclusions: These data show differentially sensitive CNS neuron subpopulations with susceptibility to low levels of ethanol. In addition, these data reveal the formation of ethanol-induced hindbrain heterotopias.

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Section: Methodsmentioning

confidence: 55%

Differentially sensitive neuronal subpopulations in the central nervous system and the formation of hindbrain heterotopias in ethanol‐exposed zebrafish

Buckley

Sidik

Kar

et al. 2019

Birth Defects Research

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“…However, recent studies using a similar ethanol exposure (2% from 6-24 hpf), found relatively minor alterations to the pattern of molecular markers of the brain (Zhang et al 2017). The patterning of the forebrain, (based on otx2 and pax6a expression) midbrain (based on fgf8a, wnt1 and pax2a), and hindbrain (based on pax6a, epha4 and, krox20) appeared largely normal, with the exception of the expression of epha4a in the rhombomere 1 boundary (Zhang et al 2017). The expression of oxt:EGFP sensitive time window is from 4-5 dpf.…”

Section: R a F Tmentioning

confidence: 92%

Diving into the world of alcohol teratogenesis: a review of zebrafish models of fetal alcohol spectrum disorder

Fernandes

Buckley

Eberhart

2018

Biochem. Cell Biol.

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The term fetal alcohol spectrum disorder (FASD) refers to the entire suite of deleterious outcomes resulting from embryonic exposure to alcohol. Along with other reviews in this special issue, we provide insight into how animal models, specifically the zebrafish, have informed our understanding of FASD. We first provide a brief introduction to FASD. We discuss the zebrafish as a model organism and its strengths for alcohol research. We detail how zebrafish has been used to model some of the major defects present in FASD. These include behavioral defects, such as social behavior as well as learning and memory, and structural defects, disrupting organs such as the brain, sensory organs, heart, and craniofacial skeleton. We provide insights into how zebrafish research has aided in our understanding of the mechanisms of ethanol teratogenesis. We end by providing some relatively recent advances that zebrafish has provided in characterizing gene-ethanol interactions that may underlie FASD.

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“…In addition to the defects in neurotransmitter systems following developmental exposure to ethanol, further alterations in brain development exist. These include altered morphology of the midbrain-hindbrain boundary (MHB), reduced expression of pax6a in the eye ( Zhang et al, 2017 ), forebrain, and hindbrain, as well as reduced expression of epha4a in rhombomere 1 of the hindbrain, which point towards altered brain development, including cerebellar development resulting from ethanol exposure. Further, early ethanol exposure has been shown to contribute to altered neurogenesis during early zebrafish development.…”

Section: Prenatal Stressmentioning

confidence: 99%

The Effects of Early Life Stress on the Brain and Behaviour: Insights From Zebrafish Models

Eachus

Choi

Ryu

2021

Front. Cell Dev. Biol.

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The early life period represents a window of increased vulnerability to stress, during which exposure can lead to long-lasting effects on brain structure and function. This stress-induced developmental programming may contribute to the behavioural changes observed in mental illness. In recent decades, rodent studies have significantly advanced our understanding of how early life stress (ELS) affects brain development and behaviour. These studies reveal that ELS has long-term consequences on the brain such as impairment of adult hippocampal neurogenesis, altering learning and memory. Despite such advances, several key questions remain inadequately answered, including a comprehensive overview of brain regions and molecular pathways that are altered by ELS and how ELS-induced molecular changes ultimately lead to behavioural changes in adulthood. The zebrafish represents a novel ELS model, with the potential to contribute to answering some of these questions. The zebrafish offers some important advantages such as the ability to non-invasively modulate stress hormone levels in a whole animal and to visualise whole brain activity in freely behaving animals. This review discusses the current status of the zebrafish ELS field and its potential as a new ELS model.

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Comparison of molecular marker expression in early zebrafish brain development following chronic ethanol or morpholino treatment

Cited by 4 publications

References 53 publications

Differentially sensitive neuronal subpopulations in the central nervous system and the formation of hindbrain heterotopias in ethanol‐exposed zebrafish

Differentially sensitive neuronal subpopulations in the central nervous system and the formation of hindbrain heterotopias in ethanol‐exposed zebrafish

Diving into the world of alcohol teratogenesis: a review of zebrafish models of fetal alcohol spectrum disorder

The Effects of Early Life Stress on the Brain and Behaviour: Insights From Zebrafish Models

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