Effect of prenatal alcohol exposure on midsagittal commissure size in rats

• Published in: Teratology (Philadelphia) Vol. 63; no. 1; p. 15
• Main Authors: Livy, D J, Elberger, A J
• Format: Journal Article
• Language: English
• Published: United States 01.01.2001
• Subjects: Alcoholism; Animals; Brain - anatomy & histology; Brain - cytology; Corpus Callosum - anatomy & histology; Disease Models, Animal; Female; Hippocampus - anatomy & histology; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; Rats; Rats, Sprague-Dawley; Regression Analysis
• ISSN: 0040-3709
• DOI: 10.1002/1096-9926(200101)63:1<15::AID-TERA1003>3.0.CO;2-Q

Fetal alcohol exposure in humans can cause a variety of brain and behavioral abnormalities. The brain abnormalities include defects in the corpus callosum that range from total absence (agenesis) to reduction in size or thickness. Determination of the critical alcohol level or time period of exposure to produce these effects is difficult because of the lack of control of possible mitigating factors. The present study was undertaken to examine possible relationships between midsagittal corpus callosum dimensions and prenatal alcohol level as measured by blood alcohol concentration, as well as prenatal period of exposure as measured by first- or second- or first- plus second-trimester equivalents in a rat model. In addition to the corpus callosum, the hippocampal and anterior commissures were also examined. Pregnant mothers were given a single daily dose of alcohol by intragastric gavage; four different doses were tested in different mothers. Peak blood alcohol concentration was determined at one of four hourly intervals thereafter. Control pregnant mothers were pairfed to individual alcohol treated mothers and handled accordingly, but no alcohol was given. Other controls consisted of normal, untreated pregnant mothers. The results show all measures of corpus callosum and anterior commissure were not affected by any dose of alcohol during any time period. However, higher BAC levels during prolonged periods of alcohol exposure were associated with reduced size of the hippocampal commissure. The results suggest that additional experimental factors not included in the present study are responsible for the effects observed in humans.