Evidence map›Paper›PMID 25522427›Full record

ArticleThe international journal of neuropsychopharmacology2014

SKF83959 produces antidepressant effects in a chronic social defeat stress model of depression through BDNF-TrkB pathway.

Bo Jiang, Fang Wang, Si Yang, Peng Fang, Zhi-Fang Deng, Jun-Li Xiao, Zhuang-Li Hu, Jian-Guo Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The international journal of neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 61 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Bo JiangDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Drs Jiang, Wang, Yang, Fang, Deng, Xiao, and Chen); Key Laboratory of Neurological Diseases (HUST), Ministry of Education of China, Wuhan, Hubei, China (Drs Wang, Hu, and Chen); The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China (Drs Wang, Hu, and Chen); The Institute of Brain Research, Huazhong University of Science and Technology, Wuhan, China (Drs Wang and Chen).
Fang WangDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Drs Jiang, Wang, Yang, Fang, Deng, Xiao, and Chen); Key Laboratory of Neurological Diseases (HUST), Ministry of Education of China, Wuhan, Hubei, China (Drs Wang, Hu, and Chen); The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China (Drs Wang, Hu, and Chen); The Institute of Brain Research, Huazhong University of Science and Technology, Wuhan, China (Drs Wang and Chen).
Si YangDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Drs Jiang, Wang, Yang, Fang, Deng, Xiao, and Chen); Key Laboratory of Neurological Diseases (HUST), Ministry of Education of China, Wuhan, Hubei, China (Drs Wang, Hu, and Chen); The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China (Drs Wang, Hu, and Chen); The Institute of Brain Research, Huazhong University of Science and Technology, Wuhan, China (Drs Wang and Chen).
Peng FangDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Drs Jiang, Wang, Yang, Fang, Deng, Xiao, and Chen); Key Laboratory of Neurological Diseases (HUST), Ministry of Education of China, Wuhan, Hubei, China (Drs Wang, Hu, and Chen); The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China (Drs Wang, Hu, and Chen); The Institute of Brain Research, Huazhong University of Science and Technology, Wuhan, China (Drs Wang and Chen).
Zhi-Fang DengDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Drs Jiang, Wang, Yang, Fang, Deng, Xiao, and Chen); Key Laboratory of Neurological Diseases (HUST), Ministry of Education of China, Wuhan, Hubei, China (Drs Wang, Hu, and Chen); The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China (Drs Wang, Hu, and Chen); The Institute of Brain Research, Huazhong University of Science and Technology, Wuhan, China (Drs Wang and Chen).
Jun-Li XiaoDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Drs Jiang, Wang, Yang, Fang, Deng, Xiao, and Chen); Key Laboratory of Neurological Diseases (HUST), Ministry of Education of China, Wuhan, Hubei, China (Drs Wang, Hu, and Chen); The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China (Drs Wang, Hu, and Chen); The Institute of Brain Research, Huazhong University of Science and Technology, Wuhan, China (Drs Wang and Chen).
Zhuang-Li HuDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Drs Jiang, Wang, Yang, Fang, Deng, Xiao, and Chen); Key Laboratory of Neurological Diseases (HUST), Ministry of Education of China, Wuhan, Hubei, China (Drs Wang, Hu, and Chen); The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China (Drs Wang, Hu, and Chen); The Institute of Brain Research, Huazhong University of Science and Technology, Wuhan, China (Drs Wang and Chen).
Jian-Guo ChenDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Drs Jiang, Wang, Yang, Fang, Deng, Xiao, and Chen); Key Laboratory of Neurological Diseases (HUST), Ministry of Education of China, Wuhan, Hubei, China (Drs Wang, Hu, and Chen); The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China (Drs Wang, Hu, and Chen); The Institute of Brain Research, Huazhong University of Science and Technology, Wuhan, China (Drs Wang and Chen). chenj@mails.tjmu.edu.cn.
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSKF83959 stimulates the phospholipase Cβ/inositol phosphate 3 pathway, resulting in the activation of Ca(2+)/calmodulin-dependent kinase IIα, which affects the synthesis of brain-derived neurotrophic factor, a neurotrophic factor critical for the pathophysiology of depression. Previous reports showed that SKF83959 elicited antidepressant activity in the forced swim test and tail suspension test as a novel triple reuptake inhibitor. However, there are no studies showing the effects of SKF83959 in a chronic stress model of depression and the role of phospholipase C/inositol phosphate 3/calmodulin-dependent kinase IIα/brain-derived neurotrophic factor pathway in SKF83959-mediated antidepressant effects.

methodsIn this study, SKF83959 was firstly investigated in the chronic social defeat stress model of depression. The changes in hippocampal neurogenesis, dendrite spine density, and brain-derived neurotrophic factor signaling pathway after chronic social defeat stress and SKF83959 treatment were then investigated. Pharmacological inhibitors and small interfering RNA/short hairpin RNA methods were further used to explore the antidepressive mechanisms of SKF83959.

resultsWe found that SKF83959 produced antidepressant effects in the chronic social defeat stress model and also restored the chronic social defeat stress-induced decrease in hippocampal brain-derived neurotrophic factor signaling pathway, dendritic spine density, and neurogenesis. By using various inhibitors and siRNA/shRNA methods, we further demonstrated that the hippocampal dopamine D5 receptor, phospholipase C/inositol phosphate 3/ calmodulin-dependent kinase IIα pathway, and brain-derived neurotrophic factor system are all necessary for the SKF83959 effects.

conclusionThese results suggest that SKF83959 can be developed as a novel antidepressant and produces antidepressant effects via the hippocampal D5/ phospholipase C/inositol phosphate 3/calmodulin-dependent kinase IIα/brain-derived neurotrophic factor pathway.

Indexed as

Social Behavior2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepineAnimalsAntidepressive AgentsBehavior, AnimalBrain-Derived Neurotrophic FactorCalcium-Calmodulin-Dependent Protein Kinase Type 2Chronic DiseaseDepressionDisease Models, AnimalDopamine AgonistsDose-Response Relationship, DrugEnzyme ActivationHippocampusInositol 1,4,5-TrisphosphateMale2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepineAntidepressive AgentsBrain-Derived Neurotrophic FactorCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, mouseDopamine AgonistsInositol 1,4,5-TrisphosphateMembrane GlycoproteinsNtrk2 protein, mouseProtein-Tyrosine KinasesReceptors, Dopamine D5Receptor, trkBRNA, Small InterferingSK&F 83959Type C Phospholipasesbrain-derived neurotrophic factorchronic social defeat stressdepressionSKF83959

Identifiers

PMID25522427
PMCPMC4438541
OpenAlexW2146737231

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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.