Figure 2

Prenatal transient systemic hypoxia-ischemia and/or intra-amniotic lipopolysaccharide leads to histological abnormalities on postnatal day 2. (A) Coronal sections from shams and each of the three insults (lipopolysaccharide (LPS) alone, transient systemic hypoxia-ischemia (TSHI) alone and TSHI + LPS) stained with H&E at P2 show the subplate (arrows) is present in shams, but less visible after the insults. Ventriculomegaly and encephalomalacia are more prominent following prenatal TSHI and TSHI + LPS, compared to shams and LPS alone. Scale bar = 100 μm. (B) Lateral ventricular volume is significantly larger in TSHI + LPS pups compared to shams (n = 3-5, ***P < 0.001). (C) Representative photomicrographs depict increased ionized calcium-binding adapter molecule 1 (Iba1) immunoreactivity in the fimbria of TSHI + LPS pups. Scale bar = 100 μm. (D) Similarly, Iba1 + load is significantly increased in TSHI + LPS pups compared to sham (n = 3-4, *P < 0.05). (E) In the fimbria, representative photomicrographs show glial fibrillary acidic protein (GFAP) immunoreactivity is also increased in TSHI + LPS pups. Scale bar = 100 μm. (F) GFAP + load in the fimbria is significantly increased in TSHI + LPS pups compared to sham (n = 3-4, **P < 0.01).