Cellular and Molecular Neurobiology
Author: Nerina Mariel Villalba | email: nvillalba@fmed.uba.ar
Nerina Villalba 1°, Catalina Madarnas 1°, Viviana Sanchez 2°, Alicia Brusco 2°
1° Universidad de Buenos Aires, CONICET, Instituto de Biología Celular y Neurociencia Prof. E. De Robertis (IBCN), Buenos Aires, Argentina.
2° Universidad de Buenos Aires, Facultad de Medicina, 1° Unidad Académica del Departamento de Histologia, Biología Celular, Embriologia y Genética, Buenos Aires, Argentina.
Perinatal ethanol exposure (PEE) impacts the developing fetus and the central nervous system being particularly affected. These alterations can have clinical implications encompassed in Fetal Alcohol Spectrum Disorders (FASD). The hippocampus is implicated in cognitive functions which are altered in adults with FASD. The dentate gyrus (DG) of the hippocampus conserves the capacity to produce new neurons in adulthood. In this context, our study aimed to describe the effect of PEE on adult hippocampal neurogenesis using a murine model. Female CD1 mice were exposed to ethanol 6% v/v along pregnancy and lactation. After weaning, pups had no further contact with ethanol. Characteristic cell types of the adult male DG were studied by immunofluorescence. A lower percentage of type 1 and 4 cells and a higher percentage of type 2 cells were observed in PEE animals. This decrease in type 1 cells suggests that PEE reduces the population of remnant progenitors of the DG present in adulthood. The increase in type 2 cells and decrease in type 4 cells may indicate that the presence of ethanol during neurodevelopment alters the capacity of neuroblasts to become neurons in the adult neurogenic niche. These results suggest that pathways implicated in cell determination were affected by PEE and remained affected in adulthood. Since neurogenesis is associated with cognitive processes altered in FASD, these results may contribute to explain one of the mechanisms involved in alcohol teratogenesis.