Direct evidence for enhanced axon sprouting in adult rats exposed to ethanol in utero.

The anterograde transport of horseradish peroxidase (HRP) was utilized to examine the post-lesion expansion of the commissural projection to the molecular layer of the dentate gyrus in adult rats prenatally exposed to ethanol, and in normal and pair-fed controls. Mean daily ethanol consumption by the pregnant dams was 12.0 +/- 1.6 g/kg. Similar consumption in a separate group of pregnant dams produced mean blood ethanol concentrations of 102.8 +/- 5.2 mg/dl of blood. The commissural terminal field of rats exposed to ethanol in utero and given unilateral entorhinal lesions as adults exhibited a significantly greater expansion compared to controls. There were no differences in the HRP-labeled terminal fields between normal and pair-fed animals with similar lesions, suggesting that the effect in the ethanol-exposed rats was due to ethanol teratogenicity rather than reduced caloric intake. Furthermore, the effect was not a function of altered organization of commissural and perforant path terminal fields (terminal field overlap). These data demonstrate that exposure to ethanol in utero produces long-lasting alterations in lesion-induced axon sprouting.