Sequence of developmental alterations following acute ethanol exposure in mice: Craniofacial features of the fetal alcohol syndrome

1983 ◽  
Vol 166 (3) ◽  
pp. 257-269 ◽  
Author(s):  
Kathleen K. Sulik ◽  
Malcolm C. Johnston
1986 ◽  
Vol 25 (S2) ◽  
pp. 97-112 ◽  
Author(s):  
Kathleen K. Sulik ◽  
Malcolm C. Johnston ◽  
Paula A. Daft ◽  
William E. Russell ◽  
Deborah B. Dehart ◽  
...  

1995 ◽  
Vol 73 (9) ◽  
pp. 1209-1223 ◽  
Author(s):  
James D. Reynolds ◽  
James F. Brien

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.


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

PEDIATRICS ◽  
1994 ◽  
Vol 93 (2) ◽  
pp. 211-215
Author(s):  
Margaret A. Pearson ◽  
Mary E. Rimsza ◽  
H. Eugene Hoyme ◽  
Laurie H. Seaver

Objective. To determine if maternal toluene abuse produces any structural or developmental disabilities in the developing fetus, a cohort of toluene-exposed infants was ascertained and examined. Methodology. Eighteen infants with a history of in utero toluene exposure were examined at birth. Nine of these infants were reexamined 3 to 36 months after their initial evaluations. The clinical findings in these patients were compared with those of similarly exposed children from the literature and with patients who had the fetal alcohol syndrome. Results. Thirty-nine percent of all toluene-exposed infants described in this and other studies were born prematurely, and 9% died during the perinatal period. Fifty-four percent were small for gestational age, and 52% exhibited continued postnatal growth deficiency. A 33% incidence of prenatal microcephaly, a 67% incidence of postnatal microcephaly, and an 80% incidence of developmental delay were observed. Eighty-three percent of the patients had craniofacial features similar to the fetal alcohol syndrome, and 89% of these children had other minor anomalies. Conclusions. Data from the patients herein described and the available scientific literature suggest that the mechanism of alcohol craniofacial teratogenesis may be nonspecific, with a variety of teratogens, including toluene, giving rise to phenotypic facial abnormalities similar to those of the fetal alcohol syndrome. We propose a common mechanism of craniofacial teratogenesis for toluene and alcohol, namely a deficiency of craniofacial neuroepithelium and mesodermal components due to increased embryonic cell death.


2004 ◽  
Vol 26 (6) ◽  
pp. 737-743 ◽  
Author(s):  
Joseph Bilotta ◽  
Jalynn A. Barnett ◽  
Laura Hancock ◽  
Shannon Saszik

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

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