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Parental care is essential for the survival of mammals, yet the mechanisms underlying its evolution remain largely unknown. Here we show that two sister species of mice, Peromyscus polionotus and Peromyscus maniculatus , have large and heritable differences in parental behaviour. Using quantitative genetics, we identify 12 genomic regions that affect parental care, 8 of which have sex-specific effects, suggesting that parental care can evolve independently in males and females. Furthermore, some regions affect parental care broadly, whereas others affect specific behaviours, such as nest building. Of the genes linked to differences in nest-building behaviour, vasopressin is differentially expressed in the hypothalamus of the two species, with increased levels associated with less nest building. Using pharmacology in Peromyscus and chemogenetics in Mus , we show that vasopressin inhibits nest building but not other parental behaviours. Together, our results indicate that variation in an ancient neuropeptide contributes to interspecific differences in parental care. Parental care in mice evolves through multiple genetic changes; one candidate is vasopressin, the reduced expression of which promotes parental nest-building behaviour in monogamous mice. Genetics of parental care Rodents display a wide range of parental care behaviours, such as nest building, with some species more driven to perform these duties than others. However, the genetic and evolutionary mechanisms that influence the extent to which parental care behaviours are performed have remained unknown. Here, Hopi Hoekstra and colleagues utilize a quantitative genetic approach to identify genetic candidates that influence parental care in closely related mouse species. Genetic changes that enhance the levels of the hypothalamic hormone vasopressin were linked to less nest building. In addition, artificial manipulation of neurons releasing vasopressin could directly affect the extent of nest building, with lower vasopressin-releasing neuronal activity correlated with increased levels of nest building. This suggests that variation in neuropeptide signalling may contribute to complex social behaviours such as parental care.

Infant cries evoke powerful responses in parents 1 – 4 . Whether parental animals are intrinsically sensitive to neonatal vocalizations, or instead learn about vocal cues for parenting responses is unclear. In mice, pup-naive virgin females do not recognize the meaning of pup distress calls, but retrieve isolated pups to the nest after having been co-housed with a mother and litter 5 – 9 . Distress calls are variable, and require co-caring virgin mice to generalize across calls for reliable retrieval 10 , 11 . Here we show that the onset of maternal behaviour in mice results from interactions between intrinsic mechanisms and experience-dependent plasticity in the auditory cortex. In maternal females, calls with inter-syllable intervals (ISIs) from 75 to 375 milliseconds elicited pup retrieval, and cortical responses were generalized across these ISIs. By contrast, naive virgins were neuronally and behaviourally sensitized to the most common (‘prototypical’) ISIs. Inhibitory and excitatory neural responses were initially mismatched in the cortex of naive mice, with untuned inhibition and overly narrow excitation. During co-housing experiments, excitatory responses broadened to represent a wider range of ISIs, whereas inhibitory tuning sharpened to form a perceptual boundary. We presented synthetic calls during co-housing and observed that neurobehavioural responses adjusted to match these statistics, a process that required cortical activity and the hypothalamic oxytocin system. Neuroplastic mechanisms therefore build on an intrinsic sensitivity in the mouse auditory cortex, and enable rapid plasticity for reliable parenting behaviour. The onset of maternal behaviour in mice involves an interaction between intrinsic tuning of auditory cortical neurons and experience-dependent plasticity.

Maternal care, including by non-biological parents, is important for offspring survival 1 – 8 . Oxytocin 1 , 2 , 9 – 15 , which is released by the hypothalamic paraventricular nucleus (PVN), is a critical maternal hormone. In mice, oxytocin enables neuroplasticity in the auditory cortex for maternal recognition of pup distress 15 . However, it is unclear how initial parental experience promotes hypothalamic signalling and cortical plasticity for reliable maternal care. Here we continuously monitored the behaviour of female virgin mice co-housed with an experienced mother and litter. This documentary approach was synchronized with neural recordings from the virgin PVN, including oxytocin neurons. These cells were activated as virgins were enlisted in maternal care by experienced mothers, who shepherded virgins into the nest and demonstrated pup retrieval. Virgins visually observed maternal retrieval, which activated PVN oxytocin neurons and promoted alloparenting. Thus rodents can acquire maternal behaviour by social transmission, providing a mechanism for adapting the brains of adult caregivers to infant needs via endogenous oxytocin. Behavioural studies and neural recordings in mice show that virgin mice can acquire maternal behaviour through an oxytocin-dependent mechanism.

Parental care improves offspring quality and survival, thereby enhancing parental fitness. Yet, seemingly maladaptive parental behaviours such as directed aggression towards the offspring have been reported in a variety of species. While maternal aggression—defined as aggressive interactions from mothers to the offspring within the family context—may be a seemingly maladaptive behaviour, it could also be an adaptive strategy allowing optimal resource allocation for current and future reproduction in the face of evolutionary conflicts of interest. This study investigated associations between maternal aggression and altered offspring development in domestic canaries ( Serinus canaria ). Offspring exposed to maternal aggression showed reduced growth, while no differences in survival were observed. In addition, juvenile males, but not females, exposed to maternal aggression displayed increased threatening behaviours, highlighting the importance of considering long-term effects when interpreting the significance of aggressive parenting styles. Females that exhibited maternal aggression did not lay larger second clutches, as would be expected if aggression during the first reproductive event was directed at prioritising future reproduction. However, they laid larger and less variable clutches overall, suggesting that females that engaged in maternal aggression may be less flexible and more prone to high investment at egg laying.

Parenting is essential for the survival and wellbeing of mammalian offspring. However, we lack a circuit-level understanding of how distinct components of this behaviour are coordinated. Here we investigate how galanin-expressing neurons in the medial preoptic area (MPOA Gal ) of the hypothalamus coordinate motor, motivational, hormonal and social aspects of parenting in mice. These neurons integrate inputs from a large number of brain areas and the activation of these inputs depends on the animal’s sex and reproductive state. Subsets of MPOA Gal neurons form discrete pools that are defined by their projection sites. While the MPOA Gal population is active during all episodes of parental behaviour, individual pools are tuned to characteristic aspects of parenting. Optogenetic manipulation of MPOA Gal projections mirrors this specificity, affecting discrete parenting components. This functional organization, reminiscent of the control of motor sequences by pools of spinal cord neurons, provides a new model for how discrete elements of a social behaviour are generated at the circuit level. Galanin-expressing neurons in the medial preoptic area coordinate different aspects of motor, motivational, hormonal and social behaviour associated with parenting by projecting to different brain regions depending on the type of behaviour and sex and reproductive state of mice.

Parental care, including feeding and protection of young, is essential for the survival as well as mental and physical well-being of the offspring. A large variety of parental behaviors has been described across species and sexes, raising fascinating questions about how animals identify the young and how brain circuits drive and modulate parental displays in males and females. Recent studies have begun to uncover a striking antagonistic interplay between brain systems underlying parental care and infant-directed aggression in both males and females, as well as a large range of intrinsic and environmentally driven neural modulation and plasticity. Improved understanding of the neural control of parental interactions in animals should provide novel insights into the complex issue of human parental care in both health and disease.

The premise that unintended childbearing has significant negative effects on the behavior of mothers and on the health of infants strongly influences public health policy and much of current research on reproductive behaviors. Yet, the evidence base presents mixed findings. Using data from the U.S. National Survey of Family Growth, we employ a measure of pregnancy intentions that incorporates the extent of mistiming, as well as the desire scale developed by Santelli et al. (Studies in Family Planning, 40, 87-100, 2009). Second, we examine variation in the characteristics of mothers within intention status groups. Third, we account for the association of mothers' background characteristics with their pregnancy intentions and with the outcomes by employing propensity score weighting. We find that weighting eliminated statistical significance of many observed associations of intention status with maternal behaviors and birth outcomes, but not all. Mistimed and unwanted births were still less likely to be recognized early in pregnancy than intended ones. Fewer unwanted births received early prenatal care or were breast-fed, and unwanted births were also more likely than intended births to be of low birth weight. Relative to births at the highest level of the desire scale, all other births were significantly less likely to be recognized early in pregnancy and to receive early prenatal care.

Exposure to severe stress has been linked to negative postpartum outcomes among new mothers including mood disorders and harsh parenting. Non-human animal studies show that stress exposure disrupts the normative adaptation of the maternal brain, thus identifying a neurobiological mechanism by which stress can lead to negative maternal outcomes. However, little is known about the impact of stress exposure on the maternal brain response to infant cues in human mothers. We examined the association of stress exposure with brain response to infant cries and maternal behaviors, in a socioeconomically diverse (low- and middle-income) sample of first-time mothers (N=53). Exposure to stress across socioeconomic, environmental, and psychosocial domains was associated with reduced brain response to infant cry sounds in several regions, including the right insula/inferior frontal gyrus and superior temporal gyrus. Reduced activation in these regions was further associated with lower maternal sensitivity observed during a mother–infant interaction. The findings demonstrate that higher levels of stress exposure may be associated with reduced brain response to an infant's cry in regions that are important for emotional and social information processing, and that reduced brain responses may further be associated with increased difficulties in developing positive mother–infant relationships.

In many species, including mice, female animals show markedly different pup-directed behaviours based on their reproductive state 1 , 2 . Naive wild female mice often kill pups, while lactating female mice are dedicated to pup caring 3 , 4 . The neural mechanisms that mediate infanticide and its switch to maternal behaviours during motherhood remain unclear. Here, on the basis of the hypothesis that maternal and infanticidal behaviours are supported by distinct and competing neural circuits 5 , 6 , we use the medial preoptic area (MPOA), a key site for maternal behaviours 7 – 11 , as a starting point and identify three MPOA-connected brain regions that drive differential negative pup-directed behaviours. Functional manipulation and in vivo recording reveal that oestrogen receptor α (ESR1)-expressing cells in the principal nucleus of the bed nucleus of stria terminalis (BNSTpr ESR1 ) are necessary, sufficient and naturally activated during infanticide in female mice. MPOA ESR1 and BNSTpr ESR1 neurons form reciprocal inhibition to control the balance between positive and negative infant-directed behaviours. During motherhood, MPOA ESR1 and BNSTpr ESR1 cells change their excitability in opposite directions, supporting a marked switch of female behaviours towards the young. ESR1-expressing cells in the principal nucleus of the bed nucleus of stria terminalis are necessary, sufficient and naturally activated during infanticide, and they form reciprocal inhibition with the maternal cells to control young-directed behaviours in female mice.

Oxytocin is a neuropeptide that is important for maternal physiology and childcare, including parturition and milk ejection during nursing 1 – 6 . Suckling triggers the release of oxytocin, but other sensory cues—specifically, infant cries—can increase the levels of oxytocin in new human mothers 7 , which indicates that cries can activate hypothalamic oxytocin neurons. Here we describe a neural circuit that routes auditory information about infant vocalizations to mouse oxytocin neurons. We performed in vivo electrophysiological recordings and photometry from identified oxytocin neurons in awake maternal mice that were presented with pup calls. We found that oxytocin neurons responded to pup vocalizations, but not to pure tones, through input from the posterior intralaminar thalamus, and that repetitive thalamic stimulation induced lasting disinhibition of oxytocin neurons. This circuit gates central oxytocin release and maternal behaviour in response to calls, providing a mechanism for the integration of sensory cues from the offspring in maternal endocrine networks to ensure modulation of brain state for efficient parenting. Experiments in mice identify a neural circuit that relays information about infant cries from the maternal auditory thalamus to hypothalamic oxytocin neurons to induce the release of oxytocin and modulate maternal behaviour.