Immunoreactivity of neurogenic factor in the guinea pig brain after prenatal hypoxia.

Chronic prenatal hypoxia is considered to cause perinatal brain injury. It can result in neurological disorders such as cerebral palsy or learning disabilities. These neurological problems are related to chronic placental insufficiency (CPI), which leads to chronic hypoxemia and hypoglycemia. The effects of hypoxia on neurogenesis during development have been a matter of controversy. We therefore investigated the effect of chronic prenatal hypoxia in the brain of the fetal guinea pig using the guinea pig CPI model. Chronic placental insufficiency was induced by unilateral uterine artery ligation at 30–32 days of gestation (dg: with term defined as ∼67dg). At 50 and 60dg, fetuses were sacrificed and assigned to either the growth-restricted (GR) or control (no ligation) group. Immunohistochemistry was performed with HIF-1α, PCNA, NeuN and BDNF antibodies in the cerebral cortex and dentate gyrus. The number of NeuN-IR and BDNF-IR cells was lesser in GR fetuses than in controls in the cerebral cortex and dentate gyrus at 60dg (p<0.05). The growth of the developing brain is dependent upon the availability of growth factors such as BDNF. The reduction in the number of neuronal cells observed in our GR group was associated with the observed reduction in BDNF protein found at 60dg. There was no significant difference between control and GR fetuses in the densities of PCNA-IR cells in the subventricular zone and subgranular zone at 50 and 60dg. These findings suggest that the survival of neurons in the cerebral cortex is decreased by chronic prenatal hypoxia at 60dg.