Optic nerve hypoplasia was detected in up to one half of a group of Swedish children born to alcoholic mothers. Using an experimental model of pre- and postnatal alcohol exposure in rats fed a liquid diet, reduced optic nerve size from gestational day 21 (294 +/- 26 x 10(2) microns2 vs 502 +/- 16 x 10(2) microns2; n = 6; p < or = 0.001) to later in development was observed as a result of the daily mean blood alcohol levels achieved in dams and their offspring. Altered glial cells and degenerating and atrophic optic axons, myelin sheaths and ganglion cells were frequent in the alcohol-exposed optic nerves. Smaller optic nerve (1.918 +/- 61 x 10(2) microns2 vs 2.195 +/- 40 x 10(2) microns2; n = 4; p < or = 0.001), reduced gaglion cell and axonal densities, and ultrastructural damage to the macroglial cells and myelin sheaths were also detected in the treated group. All these changes remained in the retina and optic nerve of the oldest rats, as a consequence of the long-lasting effects of prenatal alcohol exposure. In summary, alcohol as a major teratogenic agent may induce dysmorphogenesis and irremediable damage to the retina and optic nerve, which frequently manifests itself as hypoplastic optic nerve.