Prenatal stress on the kinetic properties of Ca 2+ and K + channels in offspring hippocampal CA3 pyramidal neurons

Abstract

Prenatal stress is known to cause neuronal loss and oxidative damage in the hippocampus of offspring rats. To further understand the mechanisms, the present study was undertaken to investigate the effects of prenatal stress on the kinetic properties of high-voltage-activated (HVA) Ca 2+ and K + channels in freshly isolated hippocampal CA3 pyramidal neurons of offspring rats. Pregnant rats in the prenatal stress group were exposed to restraint stress on days 14–20 of pregnancy three times daily for 45 min. The patch clamp technique was employed to record HVA Ca 2+ and K + channel currents. Prenatal stress significantly increased HVA Ca 2+ channel disturbance including the maximal average HVA calcium peak current amplitude (− 576.52 ± 7.03 pA in control group and − 702.05 ± 6.82 pA in prenatal stress group, p < 0.01), the maximal average HVA Ca 2+ current density (− 40.89 ± 0.31 pA/pF in control group and − 49.44 ± 0.37 pA/pF in prenatal stress group, p < 0.01), and the maximal average integral current of the HVA Ca 2+ channel (106.81 ± 4.20 nA ms in control group and 133.49 ± 4.59 nA ms in prenatal stress group, p < 0.01). The current–voltage relationship and conductance—voltage relationship of HVA Ca 2+ channels and potassium channels in offspring CA3 neurons were not affected by prenatal stress. These data suggest that exposure of animals to stressful experience during pregnancy can exert effects on calcium ion channels of offspring hippocampal neurons and that the calcium channel disturbance may play a role in prenatal stress-induced neuronal loss and oxidative damage in offspring brain.