scholarly journals Xenopus embryos to study fetal alcohol syndrome, a model for environmental teratogenesis

2018 ◽  
Vol 96 (2) ◽  
pp. 77-87 ◽  
Author(s):  
Abraham Fainsod ◽  
Hadas Kot-Leibovich
Keyword(s):  
Experimental System ◽  
Ethanol Exposure ◽  
Model Systems ◽  
Fetal Alcohol ◽  
Protein Activity ◽  
Alcohol Sensitivity ◽  
Craniofacial Malformations ◽  
Xenopus Embryos ◽  
Amphibian Embryos ◽  
Vertebrate Model

Vertebrate model systems are central to characterize the outcomes of ethanol exposure and the etiology of fetal alcohol spectrum disorder (FASD), taking advantage of their genetic and morphological closeness and similarity to humans. We discuss the contribution of amphibian embryos to FASD research, focusing on Xenopus embryos. The Xenopus experimental system is characterized by external development and accessibility throughout embryogenesis, large clutch sizes, gene and protein activity manipulation, transgenesis and genome editing, convenient chemical treatment, explants and conjugates, and many other experimental approaches. Taking advantage of these methods, many insights regarding FASD have been obtained. These studies characterized the malformations induced by ethanol including quantitative analysis of craniofacial malformations, induction of fetal growth restriction, delay in gut maturation, and defects in the differentiation of the neural crest. Mechanistic, biochemical, and molecular studies in Xenopus embryos identified early gastrula as the high alcohol sensitivity window, targeting the embryonic organizer and inducing a delay in gastrulation movements. Frog embryos have also served to demonstrate the involvement of reduced retinoic acid production and an increase in reactive oxygen species in FASD. Amphibian embryos have helped pave the way for our mechanistic, molecular, and biochemical understanding of the etiology and pathophysiology of FASD.

Fetal alcohol syndrome and DiGeorge anomaly. Critical ethanol exposure periods for craniofacial malformations as illustrated in an animal model

1986 ◽  
Vol 25 (S2) ◽  
pp. 97-112 ◽  
Author(s):  
Kathleen K. Sulik ◽  
Malcolm C. Johnston ◽  
Paula A. Daft ◽  
William E. Russell ◽  
Deborah B. Dehart ◽  
...  
Keyword(s):  
Animal Model ◽  
Fetal Alcohol Syndrome ◽  
Ethanol Exposure ◽  
Fetal Alcohol ◽  
Craniofacial Malformations ◽  
Digeorge Anomaly

Reversal of cardiomyopathy resulting from prenatal exposure to ethanol

1984 ◽  
Vol 42 ◽  
pp. 716-717
Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie
Keyword(s):  
Prenatal Exposure ◽  
Heart Development ◽  
Membrane Integrity ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Pathological Changes ◽  
Prenatally Exposed ◽  
Inner Mitochondrial Membrane ◽  
Fetal Alcohol ◽  
Newborn Mice

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.

MEMORY: VERTEBRATE MODEL SYSTEMS

1986 ◽  
pp. 299-340 ◽  
Author(s):  
Bruce S. Kapp ◽  
Jeffrey P. Pascoe
Keyword(s):  
Model Systems ◽  
Vertebrate Model

scholarly journals Müller glial cell‐dependent regeneration of the neural retina: An overview across vertebrate model systems

2016 ◽  
Vol 245 (7) ◽  
pp. 727-738 ◽  
Author(s):  
Annaïg Hamon ◽  
Jérôme E. Roger ◽  
Xian‐Jie Yang ◽  
Muriel Perron
Keyword(s):  
Glial Cell ◽  
Neural Retina ◽  
Model Systems ◽  
Müller Glial Cell ◽  
Vertebrate Model

Neurobiology of Fetal Alcohol Spectrum Disorders

2017 ◽  
Author(s):  
Carmen Lopez-Arvizu ◽  
Carmel Bogle ◽  
Harolyn M.E. Belcher
Keyword(s):  
Hormonal Regulation ◽  
Maternal Nutrition ◽  
Fetal Alcohol Spectrum Disorders ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Fetal Alcohol ◽  
Wide Range ◽  
Spectrum Disorders ◽  
The Impact ◽  
Fetal Alcohol Spectrum

Prenatal exposure to ethanol can result in a wide range of clinical presentations that are grouped under the term “Fetal Alcohol Spectrum Disorders” (FASD). The direct cellular teratogenic effects of ethanol on fetal neurodevelopment include damage to cell survival, proliferation, and migration mechanisms. Dysregulation of neurotransmission and alteration of genetic transcription have also been implicated in the neurotoxic effects of prenatal ethanol exposure. These deleterious events lead to brain volume reduction, corpus callosum dysgenesis, cerebellar, and other neuroanatomical anomalies that have been observed in individuals with FASD. Beyond direct ethanol-induced insults, the impact that ethanol has on maternal nutrition, metabolism, hormonal regulation, and placental physiology also adversely effects fetal development. The complex interactions between numerous neurobiological and psychosocial mechanisms that hinder optimal fetal neurodevelopment are reflected by the heterogeneous clinical presentation of FASD, including impaired growth, dysmorphic facial features, and cognitive and behavioral disorders.

Cholesterol homeostasis in the developing brain: a possible new target for ethanol

2007 ◽  
Vol 26 (4) ◽  
pp. 355-360 ◽  
Author(s):  
M. Guizzetti ◽  
LG Costa
Keyword(s):  
Cholesterol Synthesis ◽  
Ethanol Exposure ◽  
Developing Brain ◽  
Cholesterol Homeostasis ◽  
Fetal Alcohol ◽  
Inborn Errors ◽  
Primary Astrocyte ◽  
Glial Cell Proliferation ◽  
The Brain

Cholesterol is an essential component of cell membranes and plays an important role in signal transduction. This brief overview presents evidence from the literature that ethanol may affect cholesterol homeostasis and that, in the developing brain, this may be involved in its developmental neurotoxicity. The effects caused by inborn errors of cholesterol synthesis and by in utero ethanol exposure present several similarities in humans (eg, Smith-Lemli-Opitz syndrome and fetal alcohol syndrome), as well as in animal models. Ethanol has a cholesterol-reducing effect on the cardiovascular system, and a protective effect against Alzheimer's disease, whose pathogenesis has been linked to altered cholesterol homeostasis in the brain. In vitro, ethanol affects several functions that are mediated by cholesterol and important for brain development, such as glial cell proliferation, synaptogenesis, neuronal survival and neurite outgrowth. The brain contains high levels of cholesterol, mostly synthesized in situ. Astrocytes produce large amounts of cholesterol that can be released by these cells and utilized by neurons to form synapses. Ethanol up-regulates the cholesterol transporter ATP binding cassette A1 and cholesterol efflux from primary astrocyte cultures without affecting cholesterol synthesis. Human & Experimental Toxicology (2007) 26, 355-360

Ethanol neurobehavioural teratogenesis and the role of L-glutamate in the fetal hippocampus

1995 ◽  
Vol 73 (9) ◽  
pp. 1209-1223 ◽  
Author(s):  
James D. Reynolds ◽  
James F. Brien
Keyword(s):  
Fetal Alcohol Syndrome ◽  
Neuronal Development ◽  
Excitatory Amino Acid ◽  
Fetal Brain ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Fetal Alcohol ◽  
Current State ◽  
Developing Neurons

The purpose of this article is to review the current state of knowledge of ethanol neurobehavioural teratogenesis and its postulated mechanisms. The review comprises an examination of ethanol teratogenesis in the human, including the fetal alcohol syndrome, and in experimental animals. Several current proposed mechanisms of ethanol neurobehavioural teratogenesis are critically assessed, including the role of acetaldehyde as the proximate metabolite of ethanol; fetal hypoxia; placental dysfunction; fetal prostaglandin metabolism; and action of ethanol on developing neurons in the fetal brain, including the hippocampus, one of ethanol's main target sites. The effect of ethanol on the release of L-glutamate, an excitatory amino acid neurotransmitter, in the fetal hippocampus is described, and the role of L-glutamate in ethanol teratogenesis involving the hippocampus is discussed. A novel mechanism for abnormal neuronal development in the fetal hippocampus produced by prenatal ethanol exposure is presented, and future experiments to test this hypothesis are proposed.Key words: ethanol neurobehavioural teratogenesis, fetal alcohol syndrome, hippocampus, L-glutamate.

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