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Prenatal ethanol exposure (PEE) induces functional and structural disorders in the developing central nervous system (CNS). The relationship between radial glial cells (RGCs) and migrating neuroblasts is crucial for the establishment of normal CNS laminated structures. Pax6, a transcription factor involved in mammalian neuronal developmental processes, could be affected by PEE, as it is already known to occur in amphibians. From gestational day 10 to 18 (G10-G18), pregnant Wistar rats were subjected to an intraperitoneal injection of a daily ethanol (EtOH) 3.5 g/kg dose. Control pregnant rats received equivalent volumes of saline solution. Fetal weights and cerebral cortex thickness were significantly lower in G18 PEE than in control fetuses, and neural tube defects were found in the G18 PEE fetuses. Cortical expression of vimentin (an RGC cytoskeletal marker), S-100b protein (a neurotrophic factor and cytosolic marker of RGCs during embryonic development), and 68 kDa neurofilaments (a neuronal cytoskeletal marker) were also decreased in G18 PEE fetuses. At G14, a reduction in Pax6 cortical expression was found. Our results suggest that PEE reduces Pax6 expression in undifferentiated mammalian CNS cells. This could be one of the factors that induce RGCs and neuronal alterations at end-gestation. These alterations could be involved in the pathophysiology of neurodevelopmental disorders observed in the children affected by the fetal alcohol syndrome.

Ethanol (ETOH) exposure can result in neuronal damage. Astrocytes are morphologic and functionally related to neurons, and astrocyte‐neuron interactions provide strategic sites for the actions of many chemical compounds. The aim of the present work was to study the morphologic alterations of glial cells and neurons on the hippocampus after long‐term ETOH exposure using GFAP and S‐100β protein, neurofilaments of 200 kDa (Nf200), MAP2, and serotonin transporter (5HT‐T) immunocytochemical staining. Adult Wistar male rats (200‐250 g) were orally exposed to ETOH (6.6% v/v ad libitum) for 6 weeks. Control rats received water ad libitum. Brain sections from control and exposed rats were processed by immunocytochemistry. After ETOH exposure we observed in the CA1 area of the hippocampus: (1) an important astroglial reaction evidenced by the presence of GFAP+ reactive astrocytes; (2) an increase in S‐100β immunostaining in astroglial cells; and (3) a decrease in Nf200, 5HT‐T, and MAP2 immunoreactivity. The current study provides evidence that long‐term ETOH exposure induces alterations in the neuronal cytoskeleton and an astroglial reaction, which is a common response to brain injury and may promote functional recovery of the nervous system, as by the release of glial‐derived trophic factors (such as S‐100β) that promote cell survival and neurite growth.