Prenatal exposure to ethanol induces a relative increase in the numbers of pyramidal tract axons relative to the number of corticospinal projection neurons in somatosensory/motor cortices in the adult rat. The present study examines the effects of ethanol on the numbers of axons in the developing caudal pyramidal tract, i.e., corticospinal axons. Electron microscopic analyses of the pyramidal tracts of the offspring of pregnant rat dams fed a control diet ad libitum, pair-fed a liquid control diet, or fed an ethanol-containing diet ad libitum were performed. The pups were 5-, 15-, 30- and 90-days-old. The numbers of axons in control rats fell precipitously after postnatal day (P) 15 and the frequency of myelinated axons rose dramatically between P15 and P90. Ethanol exposure had no significant effect on the numbers of pyramidal tract axons at any age. Moreover, no ethanol-induced differences in the numbers of axons in different stages of myelination, i.e., axons that were “free” of glial associations, glia-engulfed, invested by 1–2 layers of myelin, or myelinated by 3+ layers of myelin, were detected on P15. Thus, it appears that (a) pyramidal tract axons are lost or pruned during the first two postnatal weeks and (b) postnatal development of pyramidal tract axons (e.g., pruning and myelination) is not affected by ethanol. The implications are that the ethanol-induced increase in the number of axons relative to the number of somata of corticospinal neurons detected in pups and adults results from the effects of ethanol on early stages (initiation) of axogenesis.