Maternal exposure to swainsonine impaired the early postnatal development of mouse dentate gyrus of offspring.

Neurogenesis in the dentate gyrus (DG) plays a key role in the normal of structure and function of the hippocampus-learning and memory. After eating the locoweeds, animals develop a chronic neurological disease called "locoism". Swainsonine (SW) is the main toxin in locoweeds. Studies have shown that SW induces neuronal apoptosis in vitro and impairs learning and memory in adult mouse. The present study explored effects of SW exposure to dams on the postnatal neurogenesis of DG of offspring. Pregnant ICR mice were orally gavaged with SW at a dose of 0, 5.6 or 8.4 mg/kg/day from gestation day 10 to postnatal day (PND) 21, respectively. We found that SW impaired the proliferation capacity of neural progenitor cells in the DG so that the number of newborn cells was reduced at PND 8. Using the postnatal in vivo electroporation, we showed that the dendritic branching and total length of granule cells were significantly decreased due to SW exposure. In addition, on PND 21, the density of NeuN-positive and Reelin-positive interneurons increased in the hilus, implying the disorder of neuronal migration. These results suggest that maternal exposure to SW, the neurogenesis of DG on offspring was disrupted, finally leading to the functional disorder of DG.