Optic nerve hypoplasia in an acute exposure model of the fetal alcohol syndrome.

The effects of acute prenatal exposure to ethanol on the postnatal optic nerve have been examined in a C57B1/6J mouse model. Pregnant mice were 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 gestational day and the optic nerve examined at P15. There was a significant difference in the cross-sectional areas of optic nerves from ethanol-exposed mice (Mean +/- SD: 32,800 +/- 11,000 microns2) compared to control nerves (Mean +/- SD: 52,100 +/- 8,900 microns2). 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 (ethanol group, mean of 15% myelinated axons compared to 34% for controls) in the ethanol-exposed optic nerves. There were no significant differences between experimental and control animals in the neuronal populations of the dorsal lateral geniculate nucleus and superior colliculus. This suggests that the axonal deficit is due to direct retinal damage, rather than increased postnatal axon loss arising from retinorecipient nuclei damage.