ArticleNeuron2026
Hippocampal estrogen levels, receptor types, and epigenetics contribute to sex-specific memory vulnerabilities to concurrent acute stresses.
Article in Neuron, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
- Sex-specific mechanisms of childhood trauma-related HPA axis dysregulation: Insights across four regulatory probes.Psychoneuroendocrinology · 2026Article
- Review
- Peptide signaling in the paraventricular thalamus contributes to disrupted adult reward behaviors after early-life adversity.bioRxiv : the preprint server for biology · 2026Article
- Sex-dependent serotonergic signaling across development: molecular mechanisms shaping vulnerability to neurodevelopmental and mental disorders.Frontiers in pharmacology · 2026Review
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12 authors.
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Abstract
It is increasingly recognized that acute traumatic events (e.g., mass shootings, natural disasters) can provoke enduring episodic memory deficits and generalization of trauma cues, and these are more common in women. We investigated the mechanisms and sex differences in memory vulnerability to multiple acute concurrent stresses (MACSs) in mice, focusing on the sex hormone 17β-estradiol and its receptors in the hippocampus. Surprisingly, high physiological hippocampal estradiol levels, observed in proestrus females and males, were required for MACS-induced episodic memory disruption and sensitization and generalization of stress cues. High estradiol levels were associated with permissive chromatin states in stress-vulnerable mice, while chromatin permissiveness and hippocampal estradiol were low in stress-resilient estrus females. Estrogen receptor (ER)β activation in resilient estrus females increased chromatin permissiveness and enduring vulnerability to MACSs, while ERα mediated milder stress-induced memory disruptions in males. Thus, hippocampal estradiol levels and sex modify chromatin states to enable long-lasting memory vulnerabilities to MACSs.
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