No abstract

No abstract

N-methyl-D-aspartate (NMDA) receptors are important excitatory receptors which contribute to many brain functions. Altered NMDA receptor levels cause maldevelopment of corticostriatal and corticolimbic pathways, which is a neurobiological predisposing factor for development of epilepsy, schizophrenia and other idiopathic psychotic disorders. It was hypothesized that prenatal stress could play a role in pathophysiology of these disorders by affecting expression of the receptors through releasing corticosterone. Sixty-eight virgin female Wistar rats were selected and mated with male rats with the same genotype. Then, the pregnant rats were subjected to restraint or predator stress on 15th, 16th and 17th gestation days. Prenatal stress consisted of restraint or predator stresses of the dams under normal room conditions. After parturition, the pups were studied in terms of density of NMDA receptors in brain at different time points. Meanwhile, blood sample was obtained and corticosterone blood level (CBL) was measured. The pups were then compared with the pups born to unstressed dams. Stress induced significant rise in CBL and NMDA receptors in brain of the offspring. CBL was significantly higher among the stressed rats compared to the control ones; there was significant difference between the two stresses and between the two sexes. The male pups were affected more severely. Stressful events during gestation had important effects on NMDA receptors of the offspring. It can be concluded that stress-induced elevation of NMDA receptors and corticosterone might mediate altered susceptibility to epilepsy and decrease ability of learning and memory and other stress-induced neurologic disorders.

Stress during gestation can result in early and long-term developmental aberrations. This study aimed to assess the impact of prenatal restraint or predator stress on pilocarpine-induced epileptic behavior. Pregnant rats were exposed to stressors on gestational days 15, 16, and 17. Restraint stress consisted of daily restraint of the dam. During predator stress, caged rats were exposed to a cat in a cage. On postnatal day 25, male pups were injected with pilocarpine and the behavior of each rat was observed. Prenatal stress led to low birth weight and increased blood corticosterone levels. Both stressors significantly potentiated pilocarpine-induced seizures. Predator-stressed pups exhibited significantly severe tonic-clonic seizures compared with restraint-stressed animals. These data emphasize the impact of prenatal stress on fetal growth, and neural and endocrine function. The results also suggest that psychosocial stressors have a greater impact on neural and endocrine function than physical stressors do.

No abstract