The Effects of Intrauterine Position on the Degree of Corpus Callosum Deficiency in Two Substrains of BALB/c Mice

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Douglas Wahlsten, Visiting Professor (Creator)
Institution
The University of North Carolina at Greensboro (UNCG )
Web Site: http://library.uncg.edu/

Abstract: Measures of several intrauterine position variables as well as an index of abnormality of fetal commissure development (z score) were obtained for fetuses of two substrains of BALB mice, BALB/ cWahl and BALB/cWah2, known to differ as adults in the proportion of animals exhibiting deficient corpus callosum (about 55% & 20% respectively). The extent of midline commissure development at embryonic Day 17.5 for most strain 1 fetuses was significantly reduced compared to strain 2 fetuses of the same chronological age. The two substrains also differed with respect to mean litter size and mean body weight (strain 2 > strain 1 for both measures). The ovarian and cervical positions for strain 2 uteri were found to be the most favorable for body and placental growth; no such differences were evident in strain 1. In strain 2, fetuses in the left uterine horns showed lower z scores (more retardation) than littermates on the right side, but this difference was not evident in strain I ; no other right/left differences were found in strain 2 which could help to explain the right side advantage. None of the other position variables either separately or in combination was found to be important in predicting the z score index. Tests for randomness failed to provide evidence for nonrandom distribution of severely affected fetuses. We suggest that nongenetic variability resulting from stochastic events early in development and intrinsic to the fetus may be responsible for only certain BALB fetuses within a litter exhibiting the callosal anomaly.

Additional Information

Publication
Developmental Psychobiology, 1991, 24, 395-412.
Language: English
Date: 1991
Keywords
Corpus Callosum, Mice, Heredity, Developmental factors, Deficiency, Brain structures, Physiology