Prenatal Acute Stress Attenuated Epileptiform Activities in Neonate Mice

Development of the central nervous system (CNS) is dependent on interactions between genetic and epigenetic factors, some of which could affect the susceptibility of the developing brain to damaging insults. Gestational stress has been shown as a potential factor associated with higher risk of developing certain neurological and psychiatric disorders. This study tested the hypothesis that maternal stress influences the risk of epilepsy in offsprings. Pregnant mice were exposed to restraint stress twice a day for three days at the start of the last week of gestation. Ten days after birth, the intact hippocampi of the newborn mice were excised and prepared for investigation. The hippocampi were bathed in low magnesium artificial cerebrospinal fluid to induce field potential, and the subsequent spontaneous seizure-like events of the CA1 neurons were recorded. Plasma corticosterone was measured using a commercial radioimmunoassay (RIA) kit and the values were expressed as μg/100 ml. Both the number of recurrent seizures and the duration of seizure activity were reduced in the stressed group compared to the controls (p<0.001). Stress induced a significant rise in serum corticosterone levels in both pregnant mice and in their newborn pups (p<0.001). These findings suggest that acute prenatal stress, which may mimic acute stress in human pregnancy, is a likely factor affecting seizure control in childhood temporal lobe epilepsy. The underlying inhibitory mechanism may be an increase in the level of neurosteroids both in the blood and the brain.