ArticleCurrent neurovascular research2022
Hippocampal miR-124 Participates in the Pathogenesis of Depression via Regulating the Expression of BDNF in a Chronic Social Defeat Stress Model of Depression.
Article in Current neurovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 18 citations in OpenAlex.
- Esketamine relieves postoperative depression and pain indicators in patients undergoing laparoscopic total hysterectomy.BMC anesthesiology · 2025Trial
- MicroRNA-129-5p in the mPFC is involved in the chronic mild stress-induced depression-like behaviors in rats.Acta pharmacologica Sinica · 2026Article
- Epigenetic Mechanisms of Suicidal Behavior Formation: A Review.Medical journal of the Islamic Republic of Iran · 2026Review
- MiR-134-5p/BDNF/TrkB/CREB signaling pathway involved in the depression-like behaviors in mice following exposure to benzo[a]pyrene.Metabolic brain disease · 2025Article
- Epigenetic Modifications and Neuroplasticity in the Pathogenesis of Depression: A Focus on Early Life Stress.Behavioral sciences (Basel, Switzerland) · 2024Review
- Review
- MiR-182-5p: A Novel Biomarker in the Treatment of Depression in CSDS-Induced Mice.The international journal of neuropsychopharmacology · 2024Article
- Stress, microRNAs, and stress-related psychiatric disorders: an overview.Molecular psychiatry · 2023Review
- Molecular pattern of a decrease in the rewarding effect of cocaine after an escalating-dose drug regimen.Pharmacological reports : PR · 2023Article
- Biology of cyclooxygenase-2: An application in depression therapeutics.Frontiers in psychiatry · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAs one of the most prevalent psychiatric disorders, the exact pathogenesis of depression remains elusive. Therefore, there is an urgent need to identify novel antidepressants for effective treatment. MicroRNA-124 (miR-124), the most abundant miRNA in brain tissue, plays a key effect on adult neurogenesis and neuronal differentiation. However, the mechanism of miR-124 in depression has not been clarified so far. The aim of this study is to provide broad insight into the mechanisms underlying depression.
methodsIn the study, we used the forced swim test (FST), the tail suspension test (TST), and a Chronic Social Defeat Stress (CSDS) mice model of depression. Quantitative real-time reverse transcription PCR (qRT-PCR), western blotting, immunofluorescence and virus-mediated gene transfer were used together. The level of plasma corticosterone in mice was analyzed by Enzyme Linked Immunosorbent Assay (ELISA).
resultsIt was found that CSDS robustly increased the level of miR-124 in the hippocampus. Genetic knockdown of hippocampal miR-124 produced significant antidepressant-like effects in the CSDS model of depression. Furthermore, AAV-siR-124-EGFP treatment increased the level of plasma corticosterone in CSDS-induced mice. Moreover, it was found that the antidepressant-like effects induced by miR-124 inhibition required the hippocampal BDNF-TrkB system.
conclusionHippocampal miR-124 participated in the pathogenesis of depression by regulating BDNF biosynthesis and was a feasible antidepressant target.
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.