The reduction of nNOS and ROS associated with decreased Ca2+ in hippocampus of prenatally stressed female offspring

Abstract

Prenatal stress (PS) has been known to induce oxidative damage in the offspring hippocampus. Previous researches observe that the alterations of expression of nNOS, ROS and intracellular Ca2+ in the hippocampus are advanced in the prenatally stressed female offspring rats. The objective of this study was to explore whether MK-801, a non-competitive NMDAR antagonist, could have protective effect on the oxidative stress induced by PS. Pregnant rats were randomly divided into four groups: CON group; PS group; PS+NS group; PS+MK-801 group. Eight female offspring rats were used in each group in the present experiment. Prenatally stressed rats (PS group; PS+NS group; PS+MK-801 group) exposed to restraint stress from day 14 to 20 of gestation three times daily for 45 min every time. We assayed the expression of nNOS with immunohistochemistry, ROS production with fluorescent dye Fluo3-AM dye. To measure whether intracellular Ca2+ was involved in the changes of nNOS and ROS, we also assayed the concentration of intracellular Ca2+ with DCFH-DA. Our findings showed that MK-801 lowered the increase of the nNOS expression in the hippocampus subregions and ROS in the CA3 region of female offspring, which may be relevant to the decreasing concentration of intracellular Ca2+. These results suggest that MK-801 may be associated with the protective effect on oxidative stress induced by PS.