# Neural circuit plasticity transforms infant neglect into maternal care

**Authors:** Chloe J. Bair-Marshall, Naomi L. Cassel, Ayat A. Agha, Malak Bkhiet, Robert C. Froemke

PMC · DOI: 10.21203/rs.3.rs-5983736/v1 · Research Square · 2025-02-26

## TL;DR

The study reveals how the brain adapts to transform negative emotions into caregiving behaviors in response to infant distress.

## Contribution

The research identifies a neural circuit in the central amygdala that rapidly changes to convert infant aversion into attentiveness.

## Key findings

- Initial pup contact activates CeA→LC projections, causing pup aversion.
- Oxytocin signaling in the central amygdala induces long-term depression to switch aversion to attention.
- CeA→LC projections modulate attention via corticotropin-releasing factor release onto locus coeruleus neurons.

## Abstract

Infants in distress evoke strong emotional responses in adults, which help to elicit caretaking behaviors from parents to ensure infant needs are met1–3. However, neonatal care can also be challenging, and interactions with infants can lead to stress and negative affect even in potential caregivers4–7. Child neglect and maltreatment rates in human populations make it important to understand the neural mechanisms of regulating negative emotions and stress in the parental brain8–10. Here we show how rapid plasticity in female mouse central amygdala (CeA) transforms infant aversion into attentiveness after initial pup experience. Projections from CeA to locus coeruleus (CeA→LC) were strongly activated upon initial pup contact leading to pup aversion. CeA→LC pup responses were reduced with parental experience and down-regulating CeA→LC activity led to less aversion. Oxytocin signaling in central amygdala was required to switch pup aversion to attention, inducing rapid long-term depression of excitatory inputs onto projection neurons. CeA→LC projectors released the stress hormone corticotropin-releasing factor onto LC neurons, modulating phasic firing to regulate attention. This circuit organization enables local CeA computations of pup valence to be broadcast throughout the brain by the LC central arousal system, leading to appropriate pup-directed behaviors depending on adult state.

## Linked entities

- **Proteins:** OXT (oxytocin/neurophysin I prepropeptide)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** OXT (oxytocin/neurophysin I prepropeptide) [NCBI Gene 5020] {aka OT, OT-NPI, OXT-NPI}, CRH (corticotropin releasing hormone) [NCBI Gene 1392] {aka CRF, CRH1}
- **Diseases:** depression (MESH:D003866), neglect (MESH:D058069)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11888542/full.md

## References

50 references — full list in the complete paper: https://tomesphere.com/paper/PMC11888542/full.md

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Source: https://tomesphere.com/paper/PMC11888542