High prolactin during pregnancy, which is essential for normal postpartum maternal behavior, increases neurogenesis in the subventricular zone of the lateral ventricle (SVZ) of the maternal brain. Because SVZ mitogenesis generates new olfactory neurons and may contribute to perception of novel odorants, we hypothesized that the prolactin-induced increase in SVZ mitogenesis during pregnancy might be important for normal maternal interactions with pups. To investigate this hypothesis, prolactin secretion was suppressed for 3 d early in pregnancy in mice, using a carefully timed dose of bromocriptine. The bromocriptine-induced reduction in prolactin prevented the normal increase in generation of neural progenitors in the SVZ of the maternal brain. Another group of bromocriptine-treated animals were allowed to continue their pregnancy until term, and then maternal behaviors were evaluated postpartum. Low prolactin during early pregnancy, and the consequent suppression of mitogenesis in the SVZ of the maternal brain, was subsequently followed by increased postpartum anxiety and markedly impaired maternal behavior. In another group of pregnant females, injections of the mitotic inhibitor methylazoxymethanol to specifically suppress neurogenesis in the mother during early pregnancy without affecting prolactin secretion also caused postpartum anxiety and impaired maternal behavior. These data demonstrate that prolactin-induced increase in generation of neural progenitors in the SVZ of the maternal brain during early pregnancy is required for normal expression of postpartum maternal behaviors.
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