Prenatal nicotine exposure induces depression­like behavior in adolescent female rats via modulating neurosteroid in the hippocampus.

Prenatal nicotine exposure (PNE) is closely related to depression in offspring. However, the underlying mechanism is still unclear. We hypothesized that neurosteroid in the hippocampus may mediate PNE­induced depression­like behaviors. Nicotine was subcutaneously administered (1.0 mg/kg) to pregnant rats twice daily from gestational day (GD) 9 to 20. In adolescent offspring, PNE significantly increased immobility time and decreased the sucrose preference in female rats. The numbers of hippocampal neurons declined in the CA3 and DG regions. Steroidogenic acute regulatory protein (StAR) expression was suppressed in female rats. In fetal offspring, the neuronal numbers of CA3 regions in PNE female fetal hippocampal were significantly decreased, accompanied by the enhanced content of corticosterone and StAR expression. These data indicated that PNE induced depression­like behavior in adolescent female rats via the regulation of neurosteroid levels in the hippocampus.

Epigenetic modulation during hippocampal development.

The hippocampus is located in the limbic system and is vital in learning ability, memory formation and emotion regulation, and is associated with depression, epilepsy and mental retardation in an abnormal developmental situation. Several factors have been found to modulate the development of the hippocampus, and epigenetic modification have a crucial effect in this progress. The present review summarizes the epigenetic modifications, including DNA methylation, histone acetylation, and non-coding RNAs, regulating all stages of hippocampal development, focusing on the growth of Ammons horn and the dentate gyrus in humans and rodents. These modifications may significantly affect hippocampal development and health in addition to cognitive processes.