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Published on: July 13, 2014
Prenatal ethanol exposure reduces the expression of the transcriptional factor Pax6 in the developing rat brain
María Paula Aronne1, Sergio Gustavo Evrard, Sebastián Mirochnic
1Instituto de Biología Celular y Neurociencia "Prof. Eduardo De Robertis," Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Insights
Prenatal ethanol exposure (PEE) in rats reduced fetal brain growth and caused neural tube defects. This exposure also decreased Pax6 expression, a key factor in brain development, potentially contributing to fetal alcohol syndrome disorders.
Area of Science:
- Neuroscience
- Developmental Biology
- Toxicology
Background:
- Prenatal ethanol exposure (PEE) causes central nervous system (CNS) disorders.
- Radial glial cells (RGCs) and neuroblasts are vital for CNS structure.
- Pax6, a developmental transcription factor, may be impacted by PEE.
Purpose of the Study:
- To investigate the effects of PEE on Pax6 expression and CNS development in Wistar rats.
- To determine if PEE-induced alterations in RGCs and neuroblasts contribute to neurodevelopmental disorders.
Main Methods:
- Pregnant Wistar rats received daily ethanol (EtOH) injections from gestational day 10 to 18.
- Control rats received saline injections.
- Fetal development, including weight, cerebral cortex thickness, and neural tube defects, was assessed.
- Cortical expression of vimentin, S-100b protein, 68 kDa neurofilaments, and Pax6 was analyzed.
Main Results:
- PEE significantly reduced fetal weight and cerebral cortex thickness.
- Neural tube defects were observed in PEE fetuses.
- Cortical expression of vimentin, S-100b protein, 68 kDa neurofilaments, and Pax6 was decreased in PEE fetuses.
- A reduction in Pax6 expression was noted as early as gestational day 14.
Conclusions:
- PEE negatively impacts fetal brain development, leading to structural and functional deficits.
- Reduced Pax6 expression in undifferentiated CNS cells is a potential mechanism underlying PEE-induced RGC and neuronal alterations.
- These findings suggest a link between PEE, altered Pax6 expression, and the pathophysiology of fetal alcohol syndrome.
Abstract:
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.
