Premium
Commissural size in neonatal rats: Effects of sex and prenatal alcohol exposure
Author(s) -
Zimmerberg Betty,
Scalzi Lisabeth V.
Publication year - 1989
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(89)90046-4
Subject(s) - corpus callosum , offspring , anterior commissure , sexual dimorphism , commissure , physiology , prenatal exposure , sex characteristics , medicine , pregnancy , biology , anatomy , genetics
Sex differences have been reported in the size of the adult corpus callosum in both humans and rodents. This experiment investigated whether sex and/or different prenatal treatment conditions would influence commissural size at birth. Male and female 3‐day‐old Long Evans rats were selected from one of three prenatal treatment histories: prenatal alcohol‐exposed (35% ethanol‐derived calories, 35% EDC), nutritional control (0% ethanol‐derived calories, 0% EDC) or standard control (lab chow). Midline sagittal areas of the corpus callosum and the anterior commissure were determined for these subjects. Male control subjects had significantly larger callosal areas than females. Prenatal alcohol exposure significantly abolished this sexual dimorphism, with 35% EDC males having a significantly smaller callosal area than males from both control groups. This effect was independent of prenatal treatment differences in body or brain size. There were no significant sex differences in the midline sagittal area of the anterior commissure, nor were there any apparent effects of prenatal treatment on this measure. These results indicate that sex differences in the size of the corpus callosum are present at birth. Since a difference in myelination cannot account for this difference in area, there may be a sex difference in the number of fibers or in the average fiber size. Additionally, the effects of prenatal alcohol exposure on male, but not female, offspring suggest that this alcohol‐related birth defect is hormonally mediated.