[Mechanisms of protein expression in the rat optic nerve. Modifications by alcohol exposure]

Previous work from our group demonstrated that regular high consumption of ethanol during pregnancy induces a delay in growth and structural changes in the developing eye and vision (Pinazo-Duran et al., Teratology '93; Eur J Ophthalmol '97; Stromland and Pinazo-Duran, Teratology '94; Alcohol Alcoholism '02). Our main goal is to study at a cellular and molecular level, whether or not the prenatal alcohol exposure may change the development of the glial cells and inducing the optic nerve dysmorphogenesis. We have used key protein markers to analyse the expression in the rat optic nerve throughout the pre- and postnatal periods.

To better understanding the actions of ethanol on optic nerve development in alcohol-induced and control dams, these were fed a liquid diet during gestation and lactation, containing either ethanol (5% w/, 35% of the daily food intake) or isocaloric carobydrates (35% of the daily food intake). Eyes were enucleated and processed to immunocytochemical and morphological tecnhiques and western blot approaches, using antibodies against the glial fibrillary acidid protein (GFAP), neurofilament protein (NFP) and myelin basic protein (MBP).

Three main observations were made in the ethanol-exposed and control groups: 1) the optic nerve size was significantly lower in the ethanol group than in the control group, 2) there were statistically significant changes in optic nerve astrocytes and oligodendrocytes, optic axons and myelin sheaths and 3) a delay and altered expression of developmental proteins.

All data support our earlier studies confirming the deleterious effects of ethanol on the developing visual system. We suggest that ethanol may alter the expression of precise genes involved in eye development and posterior remodelling. These results can be extrapolated to clinical advances in fetal alcohol syndrome and toxic optic neuropathies.