Number of axons in the corpus callosum of the Mature macaca nemestrina: increases caused by prenatal exposure to ethanol.

The effects of prenatal exposure to ethanol on the number of callosal axons were examined. Pregnant Macaca nemestrina were treated with ethanol (1.8 g/kg b.wt.) 1 day per week during the first 6 weeks (Et6) or full 24 weeks (Et24) of gestation. Control macaques were intubated with an isocaloric amount of sucrose water (Ct). The mid-sagittal area of the corpus callosum in 4- to 5-year-old offspring was examined in magnetic resonance (MR) images and in fixed brains. The number of callosal axons was determined by using electron microscopy. In both MR images and fixed brains of macaques treated with ethanol, the corpus callosum was 26% larger than in the controls. The rostral portion was particularly affected by ethanol; it was 55% larger in Et6- and Et24-treated macaques. Axonal size and myelin thickness were unaffected by ethanol, but ethanol-treated macaques had more callosal axons (13.7 x 10(7)) than did controls (9.4 x 10(7) axons). The increase in the rostral corpus callosum suggests that parietal and frontal cortices are particularly susceptible to ethanol. The altered callosal connectivity may be a component of the structural abnormalities that underlie executive processing problems associated with fetal alcohol syndrome. Copyright 1999 Wiley-Liss, Inc.