Fetal alcohol syndrome: Changes in craniofacial form with age, cognition, and timing of ethanol exposure in the macaque

Teratology ◽  
1999 ◽  
Vol 59 (3) ◽  
pp. 163-172 ◽  
Author(s):  
Susan J. Astley ◽  
Shannon I. Magnuson ◽  
Lena M. Omnell ◽  
Sterling K. Clarren
Keyword(s):  
Fetal Alcohol Syndrome ◽  
Ethanol Exposure ◽  
Fetal Alcohol

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

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.

Effect of gestational ethanol exposure on parvalbumin and calretinin expressing hippocampal neurons in a chick model of fetal alcohol syndrome

Alcohol ◽  
2009 ◽  
Vol 43 (2) ◽  
pp. 147-161 ◽  
Author(s):  
Audrey G. Marshall ◽  
Molly M. McCarthy ◽  
Kirk M. Brishnehan ◽  
Venugopal Rao ◽  
Lyn M. Batia ◽  
...  
Keyword(s):  
Fetal Alcohol Syndrome ◽  
Hippocampal Neurons ◽  
Ethanol Exposure ◽  
Fetal Alcohol

Ethanol exposure alters zebrafish development: A novel model of fetal alcohol syndrome

2004 ◽  
Vol 26 (6) ◽  
pp. 737-743 ◽  
Author(s):  
Joseph Bilotta ◽  
Jalynn A. Barnett ◽  
Laura Hancock ◽  
Shannon Saszik
Keyword(s):  
Fetal Alcohol Syndrome ◽  
Ethanol Exposure ◽  
Fetal Alcohol ◽  
Zebrafish Development ◽  
Novel Model

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.

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