Maternal behavior promotes resilience to adolescent stress in mice through a microglia-neuron axis DOI Creative Commons
Hongyu Chen,

Ruifeng Xu,

Jianhao Wang

et al.

Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)

Published: March 8, 2025

Early life experience modulates resilience to stress in later life. Previous research implicated maternal care as a key mediator of behavioral responses the adversity adolescence, but details molecular mechanisms remain elusive. Here, we show social activates transcription factor C/EBPβ mPFC neurons adolescent mice, which transcriptionally upregulates Dnm1l and promotes mitochondrial dysfunction, thereby conferring susceptibility mice. Moreover, different separation differentially regulates susceptibility. Mechanistically, this differential effect depends on behavior-stimulated IGF-1, inhibits neuronal through mTORC1-induced C/EBPβ-LIP translation. Furthermore, identify IGF-1 is mainly released from microglia. Notably, increased under an environmental enrichment condition or behavior impairment induced by repeated MPOAEsr1+ cells inhibition dams prevents via microglial-to-neuronal IGF-1-C/EBPβ-DRP1 signaling. In work, these findings have unveiled adolescents. Here authors that triggers microglia-derived levels, suppresses C/EBPβ-DRP1 axis, promoting

Language: Английский

Maternal behavior promotes resilience to adolescent stress in mice through a microglia-neuron axis DOI Creative Commons
Hongyu Chen,

Ruifeng Xu,

Jianhao Wang

et al.

Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)

Published: March 8, 2025

Early life experience modulates resilience to stress in later life. Previous research implicated maternal care as a key mediator of behavioral responses the adversity adolescence, but details molecular mechanisms remain elusive. Here, we show social activates transcription factor C/EBPβ mPFC neurons adolescent mice, which transcriptionally upregulates Dnm1l and promotes mitochondrial dysfunction, thereby conferring susceptibility mice. Moreover, different separation differentially regulates susceptibility. Mechanistically, this differential effect depends on behavior-stimulated IGF-1, inhibits neuronal through mTORC1-induced C/EBPβ-LIP translation. Furthermore, identify IGF-1 is mainly released from microglia. Notably, increased under an environmental enrichment condition or behavior impairment induced by repeated MPOAEsr1+ cells inhibition dams prevents via microglial-to-neuronal IGF-1-C/EBPβ-DRP1 signaling. In work, these findings have unveiled adolescents. Here authors that triggers microglia-derived levels, suppresses C/EBPβ-DRP1 axis, promoting

Language: Английский

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