The Effects of Prenatal Predator Exposure and Postnatal Environmental Enrichment on Febrile Convulsions, FosB- and CRH-immunoreactivity

Abstract

Epilepsy, a relatively common and chronic neurological condition, affects 1-2% of the population. The underlying pathophysiology of epileptogenesis is not completely understood. To identify potential antecedents to seizure, the effects of maternal stress and environmental enrichment (EE) were investigated. Maternal stress was modeled by exposing pregnant rats to a prenatal stress (PS; an ethologically relevant predatory threat). At birth, PS and naïve control (NC) dams and litters were either maintained in standard cages or transferred to EE until postnatal day (PD) 14. A model of febrile convulsions (FC) was used to determine seizure susceptibility of all offspring. Pup brains were processed for detection of FosB (FosB-ir) from structures in the limbic system and corticotrophin-releasing hormone (CRH-ir) from the paraventricular nucleus of the hypothalamus (PVN). Our results suggest pre- and postnatal dam-dependent effects. PS increased glucocorticoid (GC) levels in dams and decreased pup birth-weights. Seizure scores on PD14 were highly individualized and litter dependent, suggesting a dam-dependent and variable effect of controlled pre- and postnatal factors. EE increased FosBir within the hippocampus but, in other regions, EE decreased FosB-ir. EE also significantly decreased CRH-ir in the PVN. Our results support the concept that both preand postnatal environmental influences affect fetal programming and neurodevelopment.