Mood, Food, and Fertility: Adaptations of the Maternal Brain

Abstract

Successfully rearing young places multiple demands on the mammalian female. These are met by a wide array of alterations in maternal physiology and behavior that are coordinated with the needs of the developing young, and include adaptations in neuroendocrine systems not directly involved in maternal behavior or lactation. In this article, attenuations in the behavioral and neuroendocrine responses to stressors, the alterations in metabolic pathways facilitating both increased food intake and conservation of energy, and the changes in fertility that occur postpartum are described. The mechanisms underlying these processes as well as the factors that contribute to them and the relative contributions of these stimuli at different times postpartum are also reviewed. The induction and maintenance of the adaptations observed in the postpartum maternal brain are dependent on mother-young interaction and, in most cases, on suckling stimulation and its consequences for the hormonal profile of the mother. The peptide hormone prolactin acting on receptors within the brain makes a major contribution to changes in metabolic pathways, suppression of fertility and the attenuation of the neuroendocrine response to stress during lactation. Oxytocin is also released, both into the circulation and in some hypothalamic nuclei, in response to suckling stimulation and this hormone has been implicated in the decrease in anxiety behavior seen in the early postpartum period. The relative importance of these hormones changes across lactation and it is becoming increasingly clear that many of the adaptations to motherhood reviewed here reflect the outcome of multiple influences. © 2016 American Physiological Society. Compr Physiol 6:1493-1518, 2016.

Regulation and neurochemical identity of melanin‐concentrating hormone neurones in the preoptic area of lactating mice

“…Interestingly, behavioural expression is robustly altered during lactation . For example, lactating animals must increase their food intake to cope with the high energy demands to feed the pups, the dams increase their aggressive behaviour against intruders, sexual behaviour is temporarily inhibited and, evidently, the expression of maternal behaviour is robustly induced . Noteworthy, some key behaviours altered during lactation are also influenced by MCH, suggesting that the temporary expression of MCH in the mPOA plays a role in the transition between lactation and weaning.…”

“…1,[24][25][26] For example, lactating animals must increase their food intake to cope with the high energy demands to feed the pups, the dams increase their aggressive behaviour against intruders, sexual behaviour is temporarily inhibited and, evidently, the expression of maternal behaviour is robustly induced. 1,[24][25][26][27] Noteworthy, some key behaviours altered during lactation are also influenced by MCH, [16][17][18][19][20][21][22][23] suggesting that the temporary expression of MCH in the mPOA plays a role in the transition between lactation and weaning. Accordingly, mPOA neurones densely innervate hypothalamic nuclei that control reproduction and sexual behaviour.…”

Early life social stress and resting state functional connectivity in postpartum rat anterior cingulate circuits

“…The most substantial changes in connectivity were observed in the prefrontal cortex, nucleus accumbens, hippocampus, and somatosensory cortex, supporting the conclusion that exposure to early life CSS has persistent effects in stress, social behavior, depression, and anxiety related nuclei. Given the extensive neural plasticity related changes which occur in the female brain during gestation, parturition, and lactation (Kinsley, Bardi et al 2008; Kinsley and Lambert 2008; Hillerer, Jacobs et al 2014; Bridges 2016; Woodside 2016), it was hypothesized that CSS exposed dams would express depressed maternal care and exhibit similar (same networks), yet different specific changes in RSFC (different individual nuclei) than reported when they were adult nulliparous females (Nephew, Huang et al 2017).…”

Prolactin maintains transient melanin‐concentrating hormone expression in the medial preoptic area during established lactation

“…Another possible trigger may be the mid‐lactation decrease in circulating leptin concentrations. () Leptin receptors have been detected in the mPOA of female non‐pregnant, non‐lactating mice and rats . In the ob/ob mouse, MCH expression within the incerto‐hypothalamic and lateral hypothalamic areas is increased; hence, the mid‐lactation nadir in leptin may be responsible for up‐regulating MCH expression in the medial part of the mPOA and then prolactin maintains expression.…”