Perinatal exposure to ethanol affects postnatal degeneration and regeneration of serotoninergic pathways in the spinal cord.

It has been reported that chronic ethanol exposure during intrauterine life may cause severe adverse effects in early infancy that have been termed fetal alcohol syndrome. These alterations may perturb the normal brain development as though alcohol exposure might have altered the basic cellular interrelationship underlying neuronal plasticity. The neonatal lesion of the serotoninergic pathways in the central nervous system with the selective neurotoxin 5,7-DHT supplies an ideal model for studying the effects of substances of abuse on degenerative and regenerative events. The authors' data indicate that perinatal exposure to ethanol (3% in drinking water) causes a more rapid degeneration of the serotoninergic pathways affected by 5,7-DHT; conversely, regeneration and reinnervation of the lumbar spinal cord are markedly improved by ethanol exposure. These results suggest that perinatal ethanol exposure promotes cellular changes that at later stages are capable of improving neural repair in the brain.