Polypeptide hormones and steroid hormones, either expressed by the placenta or dependant on the placenta for their synthesis, are key to driving adaptations in the mother during pregnancy that support growth in utero. These adaptations include changes in maternal behaviour that take place in pregnancy and after the birth to ensure that offspring receive appropriate care and nutrition. Placentally-derived hormones implicated in the programming of maternal caregiving in rodents include prolactin-related hormones and steroid hormones.Neuromodulators produced by the placenta may act directly on the fetus to support brain development. A number of imprinted genes function antagonistically in the placenta to regulate the development of key placental endocrine lineages expressing these hormones. Gain-inexpression of the normally maternally expressed gene Phlda2 or loss-of-function of the normally paternally expressed gene Peg3 results in fewer endocrine cells in the placenta, and pups are born low birth weight. Importantly, wild type dams carrying these genetically altered pups display alterations in their behaviour with decreased focus on nurturing (Phlda2) or heightened anxiety (Peg3). These same genes may regulate placental hormones in human pregnancies, with the potential to influence birth weight and maternal mood. Consequently, the aberrant expression of imprinted genes in the placenta may underlie the reported cooccurrence of low birth weight with maternal prenatal depression. Key word: Placental endocrine insufficiency, imprinted genes, hormones, maternal behaviour, low birth weight, depression
Placental hormones implicated in the induction of maternal behaviourKey hormones involved in pregnancy-associated behaviours are the lactogenic hormones pituitary prolactin and prolactin-related hormones manufactured by the placenta, sometimes referred to as placental lactogens (see later). Prolactin is secreted from the pituitary to act locally on the maternal brain whereas the placentally-derived lactogenic hormones are thought to gain access to the maternal brain via the cerebrospinal fluid [14]. Key studies in rodents have experimentally demonstrated the importance of lactogenic signalling for maternal behaviour. These studies involved the infusion of prolactin or placental lactogen directly into the brains of non-pregnant animals which resulted in the stimulation of aspects postpartum maternal behaviour such as pup retrieval [14][15][16][17][18][19]. Conversely, experimentally-induced low levels of prolactin in pregnancy have been linked to increased postpartum anxiety and decreased pup retrieval [20]. Lactogenic hormones are thought to mediate their activity, at least in part, via the maternal prolactin receptor (Prlr) [21]. Loss of function of Prlr in mice was shown to result in a deficit in maternal behaviour [22,23] and, more precisely, loss of function of Prlr restricted to the medial preoptic area of the brain [24]. Signalling via Prlr is also required for the pregnancy-related increases in neurogenesis that tak...