Explore the vast range of titles available.

There is increasing recognition that perinatal anxiety disorders are both common and potentially serious for mother and child. Obsessive-compulsive disorder (OCD) can be triggered or exacerbated in the postpartum period, with mothers reporting significant effects on parenting tasks. However, there is little evidence concerning their effective treatment or the impact of successful treatment on parenting. A total of 34 mothers with OCD and a baby of 6 months old were randomized into either time-intensive cognitive-behaviour therapy (iCBT) or treatment as usual (TAU). iCBT took place after randomization at 6 months postpartum and was completed by 9 months. Maternal symptomatology, sensitivity in mother-infant interactions and parenting were assessed at baseline and reassessed at 12 months postpartum. At 12 months attachment was also assessed using Ainsworth's Strange Situation Procedure. A healthy control group of mothers and infants (n = 37) underwent the same assessments as a benchmark. iCBT was successful in ameliorating maternal symptoms of OCD (controlled effect size = 1.31-1.90). However, mother-infant interactions were unchanged by treatment and remained less sensitive in both OCD groups than a healthy control group. The distribution of attachment categories was similar across both clinical groups and healthy controls with approximately 72% classified as secure in each group. iCBT is an effective intervention for postpartum OCD. Sensitive parenting interactions are affected by the presence of postpartum OCD and this is not improved by successful treatment of OCD symptoms. However, the overall attachment bond appears to be unaffected. Longitudinal studies are needed to explore the impact of postpartum OCD as the child develops.

Although randomized interventions trials have been shown to reduce the incidence of disorganized attachment, no studies to date have identified the mechanisms of change responsible for such reductions. Maternal sensitivity has been assessed in various studies and shown to change with intervention, but in the only study to formally assess mediation, changes in maternal sensitivity did not mediate changes in infant security of attachment (Cicchetti, Rogosch, & Toth, 2006). Primary aims of the current randomized controlled intervention trial in a high-risk population were to fill gaps in the literature by assessing whether the intervention (a) reduced disorganization, (b) reduced disrupted maternal communication, and (c) whether reductions in disrupted maternal communication mediated changes in infant disorganization. The results indicated that, compared to controls (n = 52), both infant disorganization and disrupted maternal communication were significantly reduced in the intervention group (n = 65) that received regular home-visiting during pregnancy and the first year of life. Furthermore, reductions in disrupted maternal communication partially accounted for the observed reductions in infant disorganization compared to randomized controls. The results are discussed in relation to the societal cost effectiveness of early attachment-informed interventions for mothers and infants, as well as the importance of formally assessing underlying mechanisms of change in order to improve and appropriately target preventive interventions.

Cognitive bias modification (CBM) techniques, which experimentally retrain abnormal processing of affective stimuli, are becoming established for various psychiatric disorders. Such techniques have not yet been applied to maternal processing of infant emotion, which is affected by various psychiatric disorders. In a pilot study, mothers of children under 3 years old ( n  = 32) were recruited and randomly allocated to one of three training exercises, aiming either to increase or decrease their threshold of perceiving distress in a morphed continuum of 15 infant facial images. Differences between pre- and post-training threshold were analysed between and within subjects. Compared to baseline thresholds, the threshold for perceiving infant distress decreased in the lowered threshold group (mean difference −1.7 frames, 95 % confidence intervals (CI) −3.1 to −0.3, p  = 0.02), increased in the raised threshold group (1.3 frames, 95 % CI 0.6 to 2.1, p  < 0.01) and was unchanged in the control group (0.1 frames, 95 % CI −0.8 to 1.1, p  = 0.80). Between-group differences were similarly robust in regression models and were not attenuated by potential confounders. The findings suggest that it is possible to change the threshold at which mothers perceive ambiguous infant faces as distressed, either to increase or decrease sensitivity to distress. This small study was intended to provide proof of concept (i.e. that it is possible to alter a mother’s perception of infant distress). Questions remain as to whether the effects persist beyond the immediate experimental session, have an impact on maternal behaviour and could be used in clinical samples to improve maternal sensitivity and child outcomes.

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.

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.

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.

Parents know the transformative nature of having and caring for a child. Among many mammals, giving birth leads from an aversion to infant stimuli to irresistible attraction. Here, we review the biological mechanisms governing this shift in parental motivation in mammals. Estrogen and progesterone prepare the uterus for embryo implantation and placental development. Prolactin stimulates milk production, whereas oxytocin initiates labor and triggers milk ejection during nursing. These same molecules, interacting with dopamine, also activate specific neural pathways to motivate parents to nurture, bond with, and protect their offspring. Parenting in turn shapes the neural development of the infant social brain. Recent work suggests that many of the principles governing parental behavior and its effect on infant development are conserved from rodent to humans.

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.

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.

Oxytocin is important for social interactions and maternal behaviour. However, little is known about when, where and how oxytocin modulates neural circuits to improve social cognition. Here we show how oxytocin enables pup retrieval behaviour in female mice by enhancing auditory cortical pup call responses. Retrieval behaviour required the left but not right auditory cortex, was accelerated by oxytocin in the left auditory cortex, and oxytocin receptors were preferentially expressed in the left auditory cortex. Neural responses to pup calls were lateralized, with co-tuned and temporally precise excitatory and inhibitory responses in the left cortex of maternal but not pup-naive adults. Finally, pairing calls with oxytocin enhanced responses by balancing the magnitude and timing of inhibition with excitation. Our results describe fundamental synaptic mechanisms by which oxytocin increases the salience of acoustic social stimuli. Furthermore, oxytocin-induced plasticity provides a biological basis for lateralization of auditory cortical processing. A study of pup retrieval behaviour in mice shows that oxytocin modulates cortical responses to pup calls specifically in the left auditory cortex; in virgin females, call-evoked responses were enhanced, thus increasing their salience, by pairing oxytocin delivery in the left auditory cortex with the calls, suggesting enhancement was a result of balancing the magnitude and timing of inhibition with excitation. Maternal actions of oxytocin The role of oxytocin in modulating social interactions and maternal behaviour is well documented, but how this hormone influences neural circuits to drive these behavioral changes is not well understood. Here, Robert Froemke and colleagues study pup retrieval behaviour in mice and find that oxytocin modulates cortical responses to pup calls specifically in the left auditory cortex. In virgin females, call-evoked responses were enhanced, thus increasing their salience, by pairing oxytocin delivery in left auditory cortex with the calls. This enhancement came about through a specific balancing of the magnitude and timing of inhibition with excitation.