Nature Communications· 2026Q1
Elevated prenatal IL-6 levels disrupt early patterns of hippocampal electrical activity and chloride homeostasis by targeting GABAergic signaling at perinatal stage
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- 2026year
Short summary
Elevated prenatal IL-6 levels in male offspring disrupt early hippocampal electrical activity and chloride homeostasis by altering GABAergic signaling, leading to a premature shift in GABA polarity.
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Key points
- Elevated prenatal IL-6 levels disrupt early hippocampal electrical activity in male offspring.
- IL-6 alters GABAergic synaptic transmission via a STAT3-dependent pathway.
- This disruption leads to impaired chloride homeostasis and a premature shift in GABA polarity.
- The findings suggest a mechanism linking maternal inflammation to neurodevelopmental disorders in male offspring.
AI-generated from the title and abstract; the full text is not read.
Abstract
Abstract Early patterns of neuronal electrical activity are fundamental for driving critical developmental processes, including neuronal maturation and synapse formation. While genetic programs are key in orchestrating these events, the influence of environmental stressors remains poorly defined. Maternal immune activation (MIA) during pregnancy induces a systemic cytokine surge that can profoundly impact fetal brain development, increasing the risk of psychiatric and neurodevelopmental disorders. Here, we show that maternal elevation of interleukin-6 (IL-6) – a key cytokine upregulated during MIA – perturbs early hippocampal electrical activity in male offspring during the first postnatal week, a critical window for circuit formation. By triggering a STAT3-dependent modulation of early GABAergic synaptic transmission, IL-6 disrupts chloride homeostasis, causing a premature shift in the developmental GABA polarity switch. Our findings reveal a direct link between maternal immune signaling and early GABA-driven network maturation, providing insights into how inflammatory events during pregnancy may predispose male offspring to neurodevelopmental disorders.
The authors' abstract, as published at the source. Nature Communications, 2026 · DOI ↗
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Field: Biological Psychiatry
Biological PsychiatryNeuroscience