Fetal ethanol exposure: a morphometric analysis of myelination in the optic nerve

Pregnant Long-Evans rats were fed a liquid diet containing ethanol during gestation. Controls consisted of both pair-fed dams and dams fed ad libitum with an equivalent, iso-caloric diet lacking ethanol. Subsequent effects of ethanol measured in the offspring include a significant lag in the rate at which non-myelinated axons are lost in association with the initial overproduction of neurons. Additionally, there was a slight lag in the rate of acquisition of myelinated axons; and altogether there was a large increase in the ratio of non-myelinated to myelinated axons. Frequency spectra of myelinated and non-myelinated axons by size were normal, and the relationship between axon size and myelin lamellae was also normal. Measured against the dynamic, normal background of rapid cell-loss and the progressive development of myelin, morphometric demonstration and evaluation of the comparatively small divergences associated with fetal alcohol exposure are difficult: nevertheless, these results are consistent with and help account for the marginal hypomyelination previously observed by quantitative neurochemistry.