Fig. 1

Effects of prenatal exposure to LPS on pregnant mice and their offspring. A-i Schematic of the timeline of the experimental design (GD, gestation day). A-ii Birth rates of the offspring of pregnant mice with prenatal exposure to different LPS doses. Data are presented as means ± standard error mean (SEM). ***P < 0.0001 versus PBS exposure on GD 9 by one-way ANOVA with the Tukey’s multiple comparisons test. B Open filed test: Prenatal exposure to 25 µg/kg LPS on GD 9 significantly decreased the total distance travelled of the male offspring, indicating hypoactivity. Data are presented as means ± SEM. *P < 0.05 versus vehicle control by two-way ANOVA with the Tukey’s multiple comparisons test. Prenatal exposure to 25 µg/kg LPS on GD 9 significantly decreased the total distance of the male offspring. Prenatal exposure to 25 µg/kg LPS on GD 9 or 16 did not affect open arm time of the male offspring. Elevated zero maze: Prenatal exposure to 25 µg/kg LPS on GD 9 or 16 did not affect the time and entries of open arm of the male offspring. Tail suspension: Prenatal exposure to 25 µg/kg LPS on GD 9 or 16 did not affect the immobility time of the male offspring. Rotarod test: Prenatal exposure to 25 µg/kg LPS on GD 9 or 16 did not affect the latency to fall of the male offspring. Auditory brain response: Representative data of auditory brain responses of the male offspring of pregnant mice exposed to 25 µg/kg LPS on GD 9 or 16. Prenatal exposure to 25 µg/kg LPS on GD 16 significantly increased the hearing threshold of the male offspring. Data are presented as means ± SEM. *P < 0.05 versus vehicle control by two-way ANOVA with the Tukey’s multiple comparisons test. In addition, prenatal exposure to LPS did not affect the open field test times, central zone times, open arm times, or number of open arm entries, the latency to fall and auditory brain response of the female offspring