Prenatal exposure to predator odor alters placental glucocorticoid metabolism and affects fetal growth in Brandt’s voles (Lasiopodomys brandtii)

Environmental stressors encountered during pregnancy can exert profound effects on fetal development and program long-term physiological outcomes in offspring. Among these, ecologically relevant stressors such as predation risk remain understudied despite their potential to disrupt maternal physiology and placental function. In this study, we investigated how prenatal exposure to predator odor influences placental glucocorticoid (GC) metabolism and fetal growth in Brandt’s voles (Lasiopodomys brandtii). Pregnant voles were exposed to predator odor to simulate prenatal predator stress, allowing us to assess its effects on fetal growth, maternal and fetal corticosterone (CORT) levels, and the expression of key enzymes and transport proteins involved in GC regulation. The results revealed that prenatal exposure to predator odor significantly reduced fetal weight. While maternal and fetal serum CORT levels increased, placental CORT levels remained unchanged. Additionally, our study observed significant increases in the expression of placental P-glycoprotein (P-gp) and 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1), both of which are crucial for maintaining placental GC metabolic homeostasis. However, 11β-HSD2 levels were unaffected. In the fetal brain, corticotropin-releasing hormone (CRH) expression in the hypothalamus showed a downward trend, whereas glucocorticoid receptor (GR) expression in the hippocampus remained unchanged, indicating a disruption in the development of the hypothalamic-pituitary-adrenal (HPA) axis. These findings suggest that prenatal exposure to predator odor alters placental GC metabolism, leading to increased fetal CORT exposure and potentially impairing fetal development.