Effect of ethanol on the morphohistogenesis and differentiation of cerebellar granule cells in the chick embryo

Quesada, A.; Prada, Francisco A.; Espinar, Auxiliadora; Génis‐Gálvez, J. M.

doi:10.1016/0741-8329(90)90026-9

Cited by 11 publications

(2 citation statements)

References 39 publications

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“…983) according to the system of Means et al (1988). Embryos received treatment by direct injection into the yolk sac at day 6 of incubation (E6) (Chmielewski et al, 1997;Quesada et al, 1990).…”

Section: Methodsmentioning

confidence: 99%

Alcohol‐Induced Lipid and Morphological Changes in Chick Retinal Development

Aguilera

Ruı́z-Gutı́errez²,

Prada³

et al. 2004

Alcoholism Clin & Exp Res

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Section: Methodsmentioning

confidence: 99%

Alcohol‐Induced Lipid and Morphological Changes in Chick Retinal Development

Aguilera

Ruı́z-Gutı́errez²,

Prada³

et al. 2004

Alcoholism Clin & Exp Res

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“…Like mammals, alcohol-exposed chick (6.3 mg as 40% alcohol directly atop the blastodisc) displays significant apoptosis in the early brain and spinal cord (E2), and this is accompanied by reduced proliferation and cell extrusions into the neural tube lumen (as per Sandor; Giles et al 2008). Neuronal migration is similarly impaired, and their neurite extensions are fewer, shorter, and more disorganized relative to the central body and adjacent cell layers (Dow and Riopelle 1985; Kentroti and Vernadakis 1991a; Quesada et al 1990). Using the classic chick spinal cord explant, Dow and Riopelle (1985) showed that alcohol muted neurite outgrowth in response to exogenous NGF (TD50 100–170 mg%); this was not due to impaired NGF binding but to reductions in neurotrophic factor production.…”

Section: Mechanistic Insights From Avian Models Of Fasdmentioning

confidence: 99%

The avian embryo as a model for fetal alcohol spectrum disorder

Flentke

Smith

2018

Biochem. Cell Biol.

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Prenatal alcohol exposure (PAE) remains a leading preventable cause of structural birth defects and permanent neurodevelopmental disability. The chick (Gallus gallus domesticus) is a powerful embryological research model and was possibly the first (Fere, 1895) in which alcohol’s teratogenicity was demonstrated. Pharmacologically relevant alcohol exposures in the range of 20–70 mM (20–80 mg/egg) disrupt chick embryo growth, morphogenesis, and behavior, and the resulting phenotypes strongly parallel those of mammalian models. The avian embryo’s direct accessibility has enabled novel insights into alcohol’s teratogenic mechanisms. These include the contribution of IGF1 signaling to growth suppression, the altered flow dynamics that reshape valvuloseptal morphogenesis and mediate its cardiac teratogenicity, and the suppression of Wnt and Shh signals to disrupt neural crest migration, expansion, and survival and underlie its characteristic craniofacial deficits. The genetic diversity within commercial avian strains enabled identification of unique loci, such as ribosome biogenesis, that modify vulnerability to alcohol. This venerable research model is equally relevant for the future, as the application of technological advances including CRISPR, optogenetics, and biophotonics to the embryo’s ready accessibility creates a unique model in which investigators can manipulate and monitor the embryo in real-time to investigate alcohol’s actions upon cell fate.

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