From early pregnancy levels of prolactin increase dramatically, which leads to an increase in maternal gestational neurogenesis in the subventricular zone of the lateral ventricle (SVZ). As SVZ neurogenesis generates new olfactory neurons, which may contribute to perception of offspring, we hypothesized that the prolactin-induced increase in neurogenesis might be important for normal maternal behaviors. When prolactin secretion was suppressed early in pregnancy in mice, to prevent the normal increase in maternal neurogenesis, maternal anxiety was significantly increased postpartum, and maternal behavior markedly impaired. Injections of the mitotic inhibitor, methylazoxymethanol¹, to specifically suppress maternal neurogenesis without affecting prolactin secretion, also caused postpartum anxiety and impaired maternal behavior. These data demonstrated that the prolactin-induced increase in maternal SVZ neurogenesis during pregnancy is required for normal expression of postpartum maternal behaviors. In this model of postpartum anxiety we observed that daughters of anxious mothers had delayed onset of puberty. Correct levels of reproductive neurons are essential for normal reproductive physiology. Hence, we hypothesized that decreased levels of prolactin in the mother during early pregnancy alters neuronal development in offspring. Female fetuses of low prolactin (anxious) mothers had an increase in DNA methylation on day 9, but not day 7 of gestation, compared to control fetuses, demonstrating a change in the pattern of gene expression. Levels of neuronal apoptosis were increased on postnatal day 4 in both first and third generation daughters of anxious mothers, and this was associated with reduced kisspeptin expression in the hypothalamus of immature and adult female offspring. These results indicate that low levels of prolactin during early pregnancy not only significantly affect maternal behaviors, but also have a sustained and persistent effect on the reproductive physiology of female offspring.