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

Fernandes, Yohaan; Buckley, Desirè M.; Eberhart, Johann K.

doi:10.1139/bcb-2017-0122

Cited by 38 publications

(25 citation statements)

References 152 publications

(223 reference statements)

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“…While FASD is the clinical disorder caused by the maternal consumption of alcohol in humans, alcohol exposure or PAE are terms commonly used to describe embryonic development in the presence of alcohol in experimental models; mainly mouse, rat, Xenopus , zebrafish, and chick (Fainsod & Kot‐Leibovich, ; Fernandes, Buckley, & Eberhart, ; Flentke & Smith, ; Gerlai, ; Kiecker, ; Petrelli et al, ; Rojas‐Mayorquín, Padilla‐Velarde, & Ortuño‐Sahagún, ; Shabtai et al, ; Sulik & Johnston, ; Sulik, Johnston, & Webb, ). These animal models have been shown to recapitulate most of the developmental malformations characteristic of individuals with FASD.…”

Section: Experimental Vertebrate Models To Study Fasdmentioning

confidence: 99%

Insights into retinoic acid deficiency and the induction of craniofacial malformations and microcephaly in fetal alcohol spectrum disorder

Petrelli

Bendelac

Hicks

et al. 2019

Genesis

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Summary Fetal Alcohol Spectrum Disorder (FASD) is a set of neurodevelopmental malformations caused by maternal consumption of alcohol during pregnancy. FASD sentinel facial features are unique to the disorder, and microcephaly is common in severe forms of FASD. Retinoic acid deficiency has been shown to cause craniofacial malformations and microcephaly in animal models reminiscent of those caused by prenatal alcohol exposure. Alcohol exposure affects the migration and survival of cranial neural crest cells, which are required for proper frontonasal prominence and pharyngeal arch development. Defects in craniofacial development are further amplified by the many downstream pathways that are transcriptionally controlled retinoic acid target genes, including Shh signaling. Recent evidence shows that alcohol exposure itself is sufficient to induce retinoic acid deficiency in the embryo. These data suggest that retinoic acid deficiency is an important underlying etiology of FASD. In disorders like Vitamin A Deficiency, FASD, DiGeorge (22q11.2 Deletion Syndrome), CHARGE, Smith‐Magenis, Matthew‐Wood, and Congenital Zika Syndromes, evidence is accumulating to link reduced retinoic acid signaling with developmental defects like craniofacial malformations and microcephaly. Research focus on characterizing the effects of retinoic acid deficiency during early development and on understanding the downstream signaling pathways involved in aberrant head, and craniofacial development will reveal underlying etiologies of these disorders.

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Section: Experimental Vertebrate Models To Study Fasdmentioning

confidence: 99%

Insights into retinoic acid deficiency and the induction of craniofacial malformations and microcephaly in fetal alcohol spectrum disorder

Petrelli

Bendelac

Hicks

et al. 2019

Genesis

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“…Not surprisingly, alcohol exposure during these early windows can lead to a wide range of alcohol-induced facial dysmorphologies and CNS abnormalities (Sulik, 2005). CNS abnormalities are of particular interest in understanding the cognitive impact of embryonic alcohol exposure (thoroughly reviewed elsewhere [Gerlai, 2014, Fernandes, Buckley, & Eberhart, 2018). Overall, an important observation from work in animal models is that different genetic strains show different sensitivity to alcohol-induced defects, which mirrors what we see in human studies (reviewed in Eberhart & Parnell, 2016).…”

Section: Alcohol-sensitive Genes In Animal Modelsmentioning

confidence: 99%

Animal models of gene–alcohol interactions

Lovely

2019

Birth Defects Research

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Most birth defects arise from complex interactions between multiple genetic and environmental factors. However, our current understanding of how these interactions and their contributions affect birth defects remains incomplete. Human studies are limited in their ability to identify the fundamental causes of birth defects due to ethical and practical limitations. Animal models provide a great number of resources not available to human studies and they have been critical in advancing our understanding of birth defects and the complex interactions that underlie them. In this review, we discuss the use of animal models in the context of gene–environment interactions that underlie birth defects. We focus on alcohol which is the most common environmental factor associated with birth defects. Prenatal alcohol exposure leads to a wide range of cognitive impairments and structural deficits broadly termed fetal alcohol spectrum disorders (FASD). We discuss the broad impact of prenatal alcohol exposure on the developing embryo and elaborate on the current state of gene–alcohol interactions. Additionally, we discuss how animal models have informed our understanding of the genetics of FASD. Ultimately, these topics will provide insight into the use of animal models in understanding gene–environment interactions and their subsequent impact on birth defects.

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“…Animal models have been important in our understanding of the causes of FASD and multiple symptoms of FASD have been examined using zebrafish [10]. For example, growth abnormalities and craniofacial defects have been reported in zebrafish following embryonic alcohol exposure [11–13].…”

Section: Introductionmentioning

confidence: 99%

Social behavioral phenotyping of the zebrafish casper mutant following embryonic alcohol exposure

Fernandes

Rampersad

Eberhart

2019

Behavioural Brain Research

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The term Fetal Alcohol Spectrum Disorder (FASD) describes all the deleterious consequences of prenatal alcohol exposure. Impaired social behavior is a common symptom of FASD. The zebrafish has emerged as a powerful model organism with which to examine the effects of embryonic alcohol exposure on social behavior due to an innate strong behavior, called shoaling. The relative transparency of the embryo also makes zebrafish powerful for cellular analyses, such as characterizing neural circuitry. However, as zebrafish develop, pigmentation begins to obscure the brain and other tissues. Due to mutations disrupting pigmentation, the casper zebrafish strain remains relatively transparent throughout adulthood, potentially permitting researchers to image neural circuits in vivo, via epifluorescence, confocal and light sheet microscopy. Currently, however the behavioral profile of casper zebrafish post embryonic alcohol exposure has not been completed. We report that exposure to 1% alcohol from either 6 to 24, or 24 to 26 hours postfertilization reduces the social behavior of adult casper zebrafish. Our findings set the stage for the use of this important zebrafish resource in studies of FASD.

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

Cited by 38 publications

References 152 publications

Insights into retinoic acid deficiency and the induction of craniofacial malformations and microcephaly in fetal alcohol spectrum disorder

Insights into retinoic acid deficiency and the induction of craniofacial malformations and microcephaly in fetal alcohol spectrum disorder

Animal models of gene–alcohol interactions

Social behavioral phenotyping of the zebrafish casper mutant following embryonic alcohol exposure

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