ArticleScience advances2025
Enhanced Rap1 small GTPase activity in the ventral hippocampus drives stress-induced anxiety.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Unveiling the enigma of anxiety disorders and depression: from pathogenesis to treatment.Science China. Life sciences · 2026Review
- Sustained hyperactivity of parasubthalamic nucleus by PACAP signaling mediates stress-induced anxiety.Molecular psychiatry · 2026Article
- Activity of VMS-projecting mPFC neurons encodes individual vulnerability to chronic restraint stress in male mice.Neurobiology of stress · 2026Article
- Clec7a Drives Microglial Activation-Mediated Myelin Degradation in Sepsis-Associated Encephalopathy.Inflammation · 2026Article
- Emerging Potential of Ras-proximate-1 (Rap1) in Mediating Neurodegenerative Diseases.Current neuropharmacology · 2026Review
- Hippocampal NLRP3 Inflammasome Drives Anxiety- and Depressive-Like Behaviors Following Drug-Induced Liver Injury.International journal of biological sciences · 2026Article
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Authors and funding
14 authors.
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Abstract
Chronic stress exposure is a primary contributor to the development of anxiety disorders, closely associated with hippocampal dysfunction. However, the underlying molecular mechanism remains poorly understood. Here, using a mouse model of chronic restraint stress (CRS), we observed a notable increase in the activity, rather than its overall expression level, of hippocampal Rap1, a small guanosine triphosphatase belonging to the Ras superfamily. Pharmacological inhibition of Rap1 activity in the ventral hippocampus (vHPC) effectively mitigated CRS-induced anxiety. Cell type-specific manipulation of Rap1 activity revealed that Rap1 dysfunction in vHPC pyramidal neurons (PNs), but not in astrocytes or interneurons, contributed to CRS-induced anxiety-like behaviors. Mechanistically, the heightened Rap1 activity in vHPC PNs augmented their intrinsic excitability through Kv4.2 phosphorylation at the Thr
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