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.
Materials and Methods: 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.
Results: 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).
Conclusion: 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