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De Donno, C. ; Lopez, J.P.* ; Luecken, M. ; Kos, A.* ; Brivio, E.* ; Bordes, J.* ; Yang, H.* ; Deussing, J.M.* ; Schmidt, M.V.* ; Theis, F.J. ; Chen, A.*

Single-cell characterization of the adult male hippocampus suggests a prominent, and cell-type specific, role for Nrgn and Sgk1 in response to a social stressor.

Mol. Psychiatry 31, 1823-1836 (2026)
Verlagsversion Forschungsdaten DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
Stress-related psychiatric disorders impact the quality of life of half a billion people around the world. However, our understanding of the molecular mechanisms responsible for stress-response regulation remain unclear. Here, we report the largest and most comprehensive characterization of the adult male mouse hippocampus, under baseline and acute stress condition, using single-cell RNA sequencing. We further used genetically modified knockout lines for the glucocorticoid and mineralocorticoid receptors (GR and MR); two transcription factors which are pivotal regulators of the central stress-response. We found previously unknown, cell-type specific, molecular signatures of a single prolonged social defeat stress response and identified Nrgn and SgK1 as key regulators in stress-responsive glutamatergic neurons, oligodendrocytes, astrocytes, and endothelial cells. Intriguingly, GR or MR deletion, specifically in glutamatergic or GABAergic neurons, led to distinct and cell-type specific transcriptional signatures after stress exposure. This study significantly advances our understanding of the molecular and cellular network underlying the central response to stressful stimuli.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Glutamatergic ; Stressor ; Glucocorticoid Receptor ; Sgk1 ; Hippocampus ; Knockout Mouse ; Mineralocorticoid Receptor ; Gabaergic ; Social Defeat; Neurogranin; Depression; Binding; Dorsal
ISSN (print) / ISBN 1359-4184
e-ISSN 1476-5578
Zeitschrift Molecular Psychiatry
Quellenangaben Band: 31, Heft: 3, Seiten: 1823-1836 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort Campus, 4 Crinan St, London, N1 9xw, England
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Computational Biology (ICB)
Förderungen Projekt DEAL