Alcohol exposure alters the expression pattern of neural cell adhesion molecules during brain development

Neural cell adhesion molecules (NCAMs) play critical roles during developme nt of the nervous system. The aim of this study is to investigate the possi ble effect of ethanol exposure on the pattern of expression and sialylation of NCAM isoforms during postnatal rat brain development because alteration s in NCAM content and distribution have been associated with defects in cel l migration, synapse formation, and memory consolidation, and deficits in t hese processes have been observed after in utero alcohol exposure. The expr ession of NCAM isoforms in the developing cerebral cortex of pups from cont rol and alcohol-fed mothers was assessed by western blotting, ribonuclease protection assay, and immunocytochemistry. The highly sialylated form of NC AM [polysialic acid (PSA)-NCAM] is mainly expressed during the neonatal per iod and then is down-regulated in parallel with the appearance of NCAM 180 and NCAM 140, Ethanol exposure increases PSA-NCAM levels during the neonata l period, delays the loss of PSA-NCAM, decreases the amount of NCAM 180 and NCAM 140 isoforms, and reduces sialyltransferase activity during postnatal brain development. Neuraminidase treatment of ethanol-exposed neonatal bra ins leads to more intense band degradation products, suggesting a higher co ntent of NCAM polypeptides carrying PSA in these samples, However, NCAM mRN A levels are not changed by ethanol. Immunocytochemical analysis demonstrat es that ethanol triggers an increase in PSA-NCAM immunolabeling in the cyto plasm of astroglial cells, accompanied by a decrease in immunogold particle s over the plasma membrane. These findings indicate that ethanol exposure d uring brain development alters the pattern of NCAM expression and suggest t hat modification of NCAM could affect neuronal-glial interactions that migh t contribute to the brain defects observed after in utero alcohol exposure.