ArticleNature communications2025
Acute stress causes sex-specific changes to ventral subiculum synapses, circuitry, and anxiety-like behavior.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Sexually dimorphic plasticity of PV inhibition in sensory neocortex during learning.Scientific reports · 2026Article
- Sex Differences in the Ventral Subiculum's Microcircuitry and Function.Hippocampus · 2026Review
- Sex-specific gray matter underpinnings of anxiety and their mediating mechanisms inFrontiers in aging neuroscience · 2026Article
- Sex-specific GABAergic microcircuits that switch vulnerability into resilience to stress and reverse the effects of chronic stress exposure.Molecular psychiatry · 2025Article
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Abstract
Experiencing a single severe stressor is sufficient to drive sexually dimorphic psychiatric disease development. The ventral subiculum (vSUB) emerges as a site where stress may induce sexually dimorphic adaptations due to its sex-specific organization and pivotal role in stress integration. Using a 1 h acute restraint stress model in mice, we uncover that stress causes a net decrease in vSUB activity in females driven by adrenergic receptor signaling. By contrast, males exhibit a net increase in vSUB activity that is driven by corticosterone signaling. We further identified sexually dimorphic changes in vSUB output to the anterior bed nucleus of the stria terminalis and in anxiety-like behaviors in response to stress. These findings reveal striking changes in psychiatric disease-relevant brain regions and behavior following stress with sex-, cell-type, and synapse-specificity that contribute to our understanding of sexually dimorphic adaptations that may shape stress-related psychiatric disease risk.
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