OPTIC-NERVE HYPOPLASIA IN AN ACUTE EXPOSURE MODEL OF THE FETAL ALCOHOL SYNDROME

The effects of acute prenatal exposure to ethanol on the postnatal opt ic nerve have been examined in a C57B1/6J mouse model. Pregnant mice w ere exposed by intraperitoneal injection to ethanol (25% ethanol, each dose at 0.015 ml/g separated by 4 h), or to saline on the 8th gestati onal day and the optic nerve examined at P15. There was a significant difference in the cross-sectional areas of optic nerves from ethanol-e xposed mice (Mean +/- SD: 32,800 +/- 11,000 mu m(2)) compared to contr ol nerves (Mean +/- SD: 52,100 +/- 8,900 mu m(2)). This difference was mainly the result of a reduction in the number of optic nerve axons ( ethanol group, Mean +/- SD: 30,655 +/- 4,795; control group, Mean +/- SD: 45,791 +/- 5,215) but there was also deficient myelination (ethano l group, mean of 15% myelinated axons compared to 34% for controls) in the ethanol-exposed optic nerves. There were no significant differenc es between experimental and control animals in the neuronal population s of the dorsal lateral geniculate nucleus and superior colliculus. Th is suggests that the axonal deficit is due to direct retinal damage, r ather than increased postnatal axon loss arising from retinorecipient nuclei damage.