Maternal hypoxic stress such as threatened abortion at early pregnancy is thought to be a risk factor for onset of children’s neurodevelopmental disorder. In fact, we previously demonstrated that maternal stress by rearing at hypoxic condition caused communication deficit and learning disability of rat pups. To clarify the onset mechanism of neurodevelopmental disorder-like phenotype, we conducted immunohistochemical studies by using rat fetal brain. Firstly, TUNEL stain revealed that maternal hypoxic stress didn’t induce cell death. Then, immunofluorescent double staining for analyzing proliferation and differentiation of neural stem cells (NSCs) were conducted. NSCs proliferation ability analysis revealed that the rate of Ki67⁺SOX2⁺ cells were significantly increased in fetal rat brain received maternal hypoxic stress. In addition, analysis of asymmetric division which means initial step of neurogenesis, by using SOX2 and TBR2 (intermediate progenitor cell marker) double staining, showed that maternal hypoxia induced the increase of the number of NSCs. Furthermore, qPCR results showed that maternal hypoxia reduced astrogliogenesis-related genes and excitatory neurogenesis-related gene expression. This study indicated that maternal hypoxia influenced the function of NSCs and their destination.