Abstract
Fetal alcohol spectrum disorder (FASD) can cause severe mental retardation in children who are prenatally exposed to ethanol. The effects of prenatal and early postnatal ethanol exposure on adult hippocampal neurogenesis have been investigated; however, the effects of prenatal ethanol exposure on the subventricular zone (SVZ) have not. Gypenosides (GPs) have been reported to have neuroprotective effects in addition to other bioactivities. The effects of GPs on neural stem cells (NSCs) in the FASD model are unknown. Here, we test the effect of prenatal ethanol exposure on the neonatal SVZ, and the protection potential of GPs on NSCs in FASD rats. Our results show that prenatal ethanol exposure can suppress the cell proliferation and differentiation of neural stem cells in the neonatal SVZ and that GPs (400 mg/kg/day) can significantly increase the cell proliferation and differentiation of neural stem cells inhibited by ethanol. Our data indicate that GPs have neuroprotective effects on the NSCs and can enhance the neurogenesis inhibited by ethanol within the SVZ of neonatal rats. These findings provide new evidence for a potential therapy involving GPs for the treatment of FASD.
Highlights
The term fetal alcohol spectrum disorder (FASD), first defined in 1973 [1], is used to describe the developmental disorders caused by prenatal exposure to ethanol
We evaluated the effects of prenatal ethanol exposure on the neural stem cells in the neonatal subventricular zone (SVZ) and the protective effects of GPs (400 mg/kg/day) on Fetal alcohol spectrum disorder (FASD) rats
The present data provide the first evidence that prenatal ethanol exposure can suppress the cell proliferation and differentiation of neural stem cells in the neonatal SVZ and that GPs (400 mg/kg/day) can significantly increase the cell proliferation and differentiation of neural stem cells that were inhibited by ethanol
Summary
The term fetal alcohol spectrum disorder (FASD), first defined in 1973 [1], is used to describe the developmental disorders caused by prenatal exposure to ethanol. Several regions of the developing CNS are known to be affected by ethanol exposure including the cerebral cortex, hippocampus, dorsal root ganglia, and the spinal cord [4]. Neural stem cells (NSCs) are distributed in many areas in the developing brain, such as the cerebral cortex, corpus striatum, hippocampus, olfactory bulb, cerebellum and spinal cord [5]. During the end of the first trimester (gestational days-GDs 1–10 for rodents) through the second trimester (GDs 11–21/22 for mice/rats) of fetal development, NSCs produce the majority of adult neurons. This period is a specific window of vulnerability to ethanol [6]. An in vitro culture system has been used to show that
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