Relatively few behavioral deficits are apparent in subjects with hered
itary absence of the corpus callosum (CC). The anterior commissure (AC
) has been suggested to provide an extracallosal route for the transfe
r of interhemispheric information in subjects with this congenital def
ect, Anterior commissure size, axon number, axon diameter, and neurona
l distribution were compared between normal mice and those with comple
te CC absence. No difference in midsagittal AC area was found between
normals and acallosals, nor were differences found in the numbers or d
iameters of myelinated axons. However, axon counts indicated an 17% in
crease or about 70,000 more unmyelinated axons in the AC of acallosal
mice, and the mean diameter of unmyelinated axons was slightly less th
an in normal mice (0.24 vs 0.26 mu m). This decrease in axon diameter
enabled more axons to pass through the AC without increasing its midsa
gittal area. The topographical distribution of neurons sending axons t
hrough the AC, assessed with lipophilic dyes, was qualitatively simila
r for almost all the known regions of origin of the anterior commissur
e in normal and acallosal mice. There was a pronounced deficit of AC c
ells 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 t
o reach the opposite hemisphere, the higher number of axons present in
the AC of acallosal mice may contribute to the functional compensatio
n for the loss of the CC. (C) 1997 Academic Press.