Effects of ethanol exposure on myelination and axon numbers in the L2 dorsal root of the neonatal rat.

Abstract

Previous studies have demonstrated that exposure to ethanol during development delays the rate at which axons in certain central nervous system tracts acquire myelin. This delay appears to be related to an alteration in oligodendrocyte function and not to an aberrancy in axon size or number. The present study was designed to determine if alterations similar to those observed in the central nervous system also occur in peripheral nerves, specifically the L2 dorsal root. Dams were fed either an ethanol-containing or control liquid diet 2 weeks prior to pregnancy and throughout gestation. The pups born to the pregnant dams were artificially reared from postnatal day (PD) 4 to PD 10 on a similar ethanol-containing or control diet. The pups were sacrificed on PD 10, L2 dorsal roots removed and processed for electron microscopy. The numbers of axons in various states of myelination were quantified. No difference was observed in the number of unmyelinated axons in the L2 dorsal roots from ethanol-exposed and control pups. In roots from ethanol-exposed pups, there was a significant decrease in the number of axons possessing myelin arranged in compact lamellae, but a significant increase in the number of axons surrounded by myelin lamellae in which the Schwann cell cytoplasm had not yet been extruded (noncompact). However, when the number of axons possessing noncompact myelin and a compact myelin sheath were summed, no significant difference was observed. These data suggest that the delay in myelination following ethanol exposure may be a ubiquitous phenomenon throughout the nervous system.