Evidence for altered lesion-induced sprouting in the dentate gyrus of adult rats exposed to ethanol in utero.

Quantitative computer-assisted image processing techniques were used to measure changes in the Timm sulfide silver histochemical staining in the dentate gyrus of rats exposed to ethanol during gestation and following unilateral entorhinal lesions as adults. Prenatal exposure to a liquid diet containing 35% ethanol derived calories (12.6 +/- 0.9 g/kg/day) had no effect on the size of either the inner or total molecular layers. However, prenatal ethanol exposure did affect afferent reorganization when animals were lesioned as adults. There was a significant increase in the width and area of the inner molecular layer compared to control rats with similar lesions. The increase was interpreted as an exaggerated post-lesion expansion of the commissural/associational fibers. This alteration of a stereotypic sprouting response was not a general effect; no change was observed in mossy fiber sprouting in the dentate gyrus. These findings suggest that heavy maternal ethanol consumption can have long-lasting consequences on the developing central nervous system, but that such effects are not common to every form of axon sprouting.