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Abstract:Inbred mouse strains that lack the corpus callosum connecting the cerebral hemispheres in the adult differ from the C57BL/6J strain at several relevant but unknown loci. To identify at least one major locus that influences axon guidance, different strains showing phenotypically similar defects were crossed to test for allelism. It the F 1 hybrid between two strains with the same brain defect is phenotypically normal, it is much more likely that the two strains will differ at fewer loci than will an acallosal strain and C57BL/6J. This approach proved to be very informative. Five reasonable models of inheritance involving two or three loci were assessed, and the data justified rejection of all but one hypothesis. A total of 479 mice were obtained from tour inbred strains prone to absence of the corpus callosum (BALB/cWah 1, BALB/cWah2,

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Abstract:Relatively few behavioral deficits are apparent in subjects with hereditary absence of the corpus callosum (CC). The anterior commissure (AC) has been suggested to provide an extracallosal route for the transfer of interhemispheric information in subjects with this congenital defect. Anterior commissure size, axon number, axon diameter, and neuronal distribution were compared between normal mice and those with complete CC absence. No difference in midsagittal AC area was found between normals and acallosals, nor were differences found in the numbers or diameters of myelinated axons. However, axon counts indicated an 17%increase or about 70,000 more unmyelinated axons in the AC of acallosal mice, and the mean diameter of unmyelinated axons was slightly less than in normal mice (0.24 vs 0.26 μm). This decrease in axon diameter enabled more axons to pass through the AC without increasing its midsagittal area. The topographical distribution of neurons sending axons through the AC, assessed with lipophilic dyes, was qualitatively similar for almost all the known regions of origin of the anterior commissure in normal and acallosal mice. There was a pronounced deficit of AC cells in the anterior piriform cortex of BALB/c mice, but this occurred whether or not the mouse suffered absent CC. Although the increase in AC axon number is far smaller than the number of CC axons that fail to reach the opposite hemisphere, the higher number of axons present in the AC of acallosal mice may contribute to the functional compensation for the loss of the CC.

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