Preimplantational ethanol exposure causes disturbances in gene expression and abnormalities in cerebral cortex morphogenesis and behavior.

Abstract

Preimplantational ethanol exposure during the early stages of pregnancy is associated with significant developmental abnormalities in the cerebral cortex and behavioral changes. This study explores the impact of such exposure on neurogenesis, cortical morphogenesis, neuronal development, and behavioral outcomes. Ethanol exposure impairs the proliferation of radial glial and intermediate progenitor cells, disrupting neurogenesis in the dorsal telencephalon. Histological analysis reveals reduced neuronal distribution and decreased microglia numbers, highlighting neuroinflammation's role in these abnormalities. Gene expression studies show disrupted BDNF expression and upregulation of neurogenesis-related genes like Ngn2 and NeuroD, suggesting a potential imbalance in neuronal differentiation. Behavioral assessments in postnatal mice indicate significant impairments in locomotor and psychomotor activities and altered social proximity, though overall social interaction remains largely unchanged. Observations from open field tests demonstrate reduced spontaneous and psychomotor activity in alcohol-exposed mice. In multi-individual settings, these mice show decreased inter-individual distance, suggesting altered social proximity preferences. These findings underscore the long-term consequences of early prenatal ethanol exposure on brain development and behavior. The disruption in cortical morphogenesis, along with neuroinflammation and altered gene expression, is linked to neurodevelopmental deficits characteristic of fetal alcohol spectrum disorders (FASD). 10205Further studies are necessary to better understand the mechanisms involved and mitigate long-term impacts.