ArticleTranslational psychiatry2016
Role of hippocampal p11 in the sustained antidepressant effect of ketamine in the chronic unpredictable mild stress model.
Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 86 citations in OpenAlex.
- Disruptions of p11 (S100A10) and HPA Axis Homeostasis Participate in the Major Depressive Disorder (MDD) Especially in Female Patients.Neuropsychiatric disease and treatment · 2025Trial
- Investigation of Potential Therapeutic Effects of New Rapid-Acting Antidepressant Drugs (RAADs) Using Stress-Based Models of Depression.Biomolecules · 2026Review
- (R)-ketamine induces mGluPsychopharmacology · 2025Article
- Are "mystical experiences" essential for antidepressant actions of ketamine and the classic psychedelics?European archives of psychiatry and clinical neuroscience · 2025Review
- Evaluation of behavioural and neurochemical effects of psilocybin in mice subjected to chronic unpredictable mild stress.Translational psychiatry · 2025Article
- Depression-like effects induced by chronic unpredictable mild stress in mice are rapidly reversed by a partial negative allosteric modulator of mGluPsychopharmacology · 2025Article
- Enduring modulation of dorsal raphe nuclei regulates (R,S)-ketamine-mediated resilient stress-coping behavior.Molecular psychiatry · 2025Article
- Ketamine Reduces Avoidance Responses During Re-Exposition to Aversive Stimulus: Comparison Between (Brain sciences · 2024Article
- Ketamine and its two enantiomers in anesthesiology and psychiatry: A historical review and future directions.Journal of anesthesia and translational medicine · 2024Review
- Brain region-specific action of ketamine as a rapid antidepressant.Science (New York, N.Y.) · 2024Article
- Partial mGluPharmacological reports : PR · 2024Article
- Chronic Stress-Induced Elevation of Melanin-Concentrating Hormone in the Locus Coeruleus Inhibits Norepinephrine Production and Associated With Depression-Like Behaviors in Rats.The international journal of neuropsychopharmacology · 2024Article
- Ahnak in the prefrontal cortex mediates behavioral correlates of stress resilience and rapid antidepressant action in mice.Frontiers in molecular neuroscience · 2024Article
- Reduction of p11 in dorsal raphe nucleus serotonergic neurons mediates depression-like behaviors.Translational psychiatry · 2023Article
- Role of P11 through serotonergic and glutamatergic pathways in LID.Molecular biology reports · 2023Review
- Role of the mesolimbic dopamine pathway in the antidepressant effects of ketamine.Neuropharmacology · 2023Review
- Combined Administration of (Pharmaceuticals (Basel, Switzerland) · 2022Article
- Update on GPCR-based targets for the development of novel antidepressants.Molecular psychiatry · 2022Review
- S100A10 and its binding partners in depression and antidepressant actions.Frontiers in molecular neuroscience · 2022Review
- Ketamine-50 years in use: from anesthesia to rapid antidepressant effects and neurobiological mechanisms.Pharmacological reports : PR · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although ketamine shows a rapid and sustained antidepressant effect, the precise mechanisms underlying its effect are unknown. Recent studies indicate a key role of p11 (also known as S100A10) in depression-like behavior in rodents. The present study aimed to investigate the role of p11 in the antidepressant-like action of ketamine in chronic unpredictable mild stress (CUMS) rat model. The open-field test, forced swimming test and sucrose preference test were performed after administration of ketamine (10 mg kg(-1)) or a combination of ketamine and ANA-12 (a tropomyosin-related kinase B (TrkB) antagonist; 0.5 mg kg(-1)). The lentivirus vector for p11 was constructed to knock down the hippocampal expression of p11. In the CUMS rats, ketamine showed a rapid (0.5 h) and sustained (72 h) antidepressant effect, and its effect was significantly blocked by co-administration of ANA-12. Furthermore, ketamine significantly increased the reduced expression of brain-derived neurotrophic factor (BDNF) in the hippocampus of CUMS rats, whereas ketamine did not affect the expression of p11 in CUMS rats 0.5 h after administration. In addition, ketamine significantly increased the reduced ratio of p-TrkB/TrkB in the hippocampus by CUMS rats, and its effect was also blocked by ANA-12. Moreover, the reduced expression of BDNF and p11 in the hippocampus of CUMS rats was significantly recovered to control levels 72 h after ketamine administration. Interestingly, knockdown of hippocampal p11 caused increased immobility time and decreased sucrose preference, which were not improved by ketamine administration. These results suggest that p11 in the hippocampus may have a key role in the sustained antidepressant effect of ketamine in the CUMS model of depression.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.