E Ozer1, S Sarioglu, A Güre. 1. Department of Pathology, Dokuz Eylül University School of Medicine, Izmir, Turkey.
Abstract
BACKGROUND: One of the most severe consequences of maternal alcohol consumption is the damage to the developing central nervous system. MATERIAL AND METHODS: To evaluate the effect of prenatal alcohol exposure on neuronal migration, neuronogenesis and myelination in the brain, pregnant BALB/C mice were maintained on either liquid diets containing ethanol (12 g/kg body weight) beginning on gestation day 6 or isocoloric diet (control group). The dams were sacrificed on gestation day 17 and the brain sections of the pups were analyzed using immunohistochemical method to evaluate the number of neurons, oligodendrioglial expression of myelin basic protein (MBP) and neuronal expression of neural cell adhesion molecule (NCAM). RESULTS: Ethanol-exposed pups revealed significantly weaker expression of MBP compared to the control group. In contrast, no significant difference of NCAM expression and neuronal cell count were present between ethanol-exposed pups and the control group. CONCLUSION: These data demonstrate that alcohol exposure affects the level of MBP expression, consequently causing a reduction in brain myelination that may lead to neuronal dysfunction. The ineffectiveness of prenatal alcohol exposure on the number of neurons in contrast to the previous reports might be due to the adequate sampling of areas for cell counting. Although there is a view that NCAM is involved both directly and indirectly in neuronal cell migration, we speculate that alcohol neuroembryotoxicity uncouples this relationship. Other adhesion molecules, such as L1, or extracellular matrix proteins, such as laminin, would be other candidates for investigation.
BACKGROUND: One of the most severe consequences of maternal alcohol consumption is the damage to the developing central nervous system. MATERIAL AND METHODS: To evaluate the effect of prenatal alcohol exposure on neuronal migration, neuronogenesis and myelination in the brain, pregnant BALB/C mice were maintained on either liquid diets containing ethanol (12 g/kg body weight) beginning on gestation day 6 or isocoloric diet (control group). The dams were sacrificed on gestation day 17 and the brain sections of the pups were analyzed using immunohistochemical method to evaluate the number of neurons, oligodendrioglial expression of myelin basic protein (MBP) and neuronal expression of neural cell adhesion molecule (NCAM). RESULTS:Ethanol-exposed pups revealed significantly weaker expression of MBP compared to the control group. In contrast, no significant difference of NCAM expression and neuronal cell count were present between ethanol-exposed pups and the control group. CONCLUSION: These data demonstrate that alcohol exposure affects the level of MBP expression, consequently causing a reduction in brain myelination that may lead to neuronal dysfunction. The ineffectiveness of prenatal alcohol exposure on the number of neurons in contrast to the previous reports might be due to the adequate sampling of areas for cell counting. Although there is a view that NCAM is involved both directly and indirectly in neuronal cell migration, we speculate that alcohol neuroembryotoxicity uncouples this relationship. Other adhesion molecules, such as L1, or extracellular matrix proteins, such as laminin, would be other candidates for investigation.
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