Genetic and developmental defects of the mouse corpus callosum

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Abstract
Among adult BALB mice fewer than 20% usually have a small or absent corpus callosum (CC) and inheritance is polygenic. In the fetus at the time when the CC normally forms, however, almost all BALB mice show a distinct bulge in the interhemispheric fissure and grossly retarded commissure formation, and inheritance appears to result from two autosomal loci, provided the overall maturity of fetuses is equated. Most fetuses recover from the early defect when the CC axons manage to cross over the hippocampal commissure, and thus there is developmental compensation for a genetic defect rather than arrested midline development. The pattern of interhemispheric connections when the adult CC is very small is topographically normal in most respects, despite the unusual paths of the axons. The proportion of mice which fail to recover completely can be doubled by certain features of the maternal environment, and the severity of defects in adults can also be exacerbated by new genetic mutations which create new BALB substrains. The behavioral consequences of absent CC in mice are not known, nor have electrophysiological patterns been examined. The mouse provides an important model for prenatal ontogeny and cortical organization in human CC agenesis, because these data are not readily available for the human condition.