Placental Regulation Of Maternal Endocrine Function And Behavior

The placenta, developed from the cell lineage of fetal trophectoderm, exerts considerable influence on maternal endocrine function. Progesterone is the steroid hormone that dominates pregnancy and is necessary to sustain pregnancy. High levels of progesterone during pregnancy are a function of the fetal placenta either directly (primates) or indirectly (rodents) by production of placental hormones that sustain the ovarian corpus luteum. Progesterone has a broad spectrum of effects by acting on many maternal tissues (Keverne, 2006). Notable among these is the brain, particularly the hypothalamus (Fig. 8.1). In the hypothalamic region of the brain, high levels of progesterone exert a negative feedback on the pulsatile release of gonadotropin-releasing hormone (GnRH) preventing ovulatory cycles and curtailing female sexual behavior. The GnRH neurons are not themselves steroid receptive cells but it is thought that negative feedback inhibition occurs via the action of steroids on 7-aminobutyric acid (GABA-ergic) interneurons (Everitt and Keverne, 1986). GnRH results in the release of luteinizing hormone (LH) from the anterior pituitary, which is essential for folliculogenesis and reactivation of the reproductive cycle. In most mammalian species, progesterone-negative feedback inhibits folliculogenesis and hence oestrogen production, thereby resulting in a complete suppression of female fertility and sexual receptivity. In the large-brained primates, where sexual receptivity has become substantially emancipated from endocrine determinants, high levels of progesterone in pregnancy still reduce sexual activity but

Figure 8.1. Placentally regulated steroids: multiple effects on maternalism.

mainly as a consequence of the peripheral actions of this hormone on the reproductive tract and sexual skin swellings (Keverne, 1984).

Placental progesterone is important not only in suppressing pregnant female sexual behavior but also for priming the brain for promotion of maternal behavior. Other placental hormones of importance in the context of maternal behavior are prolactin and oestrogen. In the late stages of pregnancy, prior to parturition and the onset of maternal behavior, notable changes occur in the circulating levels of hormones in the female which have much in common across most mammalian species studied. These changes involve a fall in progesterone levels and an increase in oestrogen and prolactin, maternal endocrine changes that are dependent on the placenta. Prolactin-like hormones produced by the trophectoderm cell lineages become the primary luteotropins in the latter third of rodent pregnancy and peak in the maternal circulation at parturition (Grattan, 2002). Oestrogen levels that increase toward the end of pregnancy are also directly dependent on the placenta. Placental trophoblast cells are the major site for conversion of progestins into androgen, which then serves as the precursor for aromatization to oestrogen by the maternal ovary. In the female rodent brain, placental lactogens (PL-I and PL-II) have been shown to promote maternal behavior by priming the brain possibly by an action on dopamine neurons (Mann and Bridges, 2001). Progesterone and oestrogen are steroids that readily permeate the blood-brain barrier and both of these hormones have effects on oxytocinergic neurons. Oxytocin is produced in the hypothalamic (paraventricular) parvocellular neurons to activate maternal behavior, while the magnocellular production of oxytocin is important for parturition and milk letdown. High levels of progesterone promote oxytocin synthesis but inhibit neural firing and hence oxytocin release (Kendrick and Keverne, 1992). Around the time of parturition, the falling levels of progesterone and increasing levels of oestrogen promote the synthesis of oxytocin receptors in the brain, uterus, and mammary gland (Broad et al., 1999; Johnson et al., 1989). Hence, the conceptus, via the hormones of its extraembryonic trophectoderm, capitalizes on the maternal neuroendocrine system to determine its own destiny by ensuring the synchronization of birth with milk letdown and maternal care. In order to ensure fetal control over the timing of parturition, the placental trophoblast cell lineage silences the firing of maternal oxytocinergic neurons by producing or inducing high levels of progesterone. Any prepartum oxytocin leakage from the posterior pituitary is taken care of by a proteolytic enzyme (oxytocinase) again produced by the placenta, rendering this oxytocin biologically inactive.

In addition to the production of prolactin under the regulatory control of the placental genome, the maternal pituitary also produces prolactin. This is under the secretory control of the maternal hypothalamus via the tuberoinfun-dibular dopamine neurons, the release of dopamine acting as a prolactin inhibitory factor on the pituitary lactotrophs. During pregnancy, these lactotrophs are primed for prolactin production by progesterone which induces dephosphoryla-tion and inactivation of tyrosine hydroxylase, the precursor of dopamine (Arbogast and Voogt, 2002). Thus, the placenta by both a direct placental and indirect maternal action via the hypothalamus ensures that the mammary gland is well provided with milk in readiness for birth as well as providing a means of sustaining this production after the placenta is lost.

Pregnancy Nutrition

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