Evidence map›Paper›PMID 32864894›Full record

ArticleCNS neuroscience & therapeutics2021

Genetic and pharmacological inhibition of two-pore domain potassium channel TREK-1 alters depression-related behaviors and neuronal plasticity in the hippocampus in mice.

Fangfang Wu, Hongbin Sun, Weigang Gong, Xiaoli Li, Zhaohui Pan, Han Shan, Zhijun Zhang

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. The Inhibition of TREK-1 KInternational journal of molecular sciences · 2024
    Article
  11. Neural plasticity and depression treatment.IBRO neuroscience reports · 2023
    Article
  12. Article
  13. Noninvasive Delivery of Biologicals to the Brain.Focus (American Psychiatric Publishing) · 2022
    Article
  14. Article
  15. Review
  16. GW117: A novel serotonin (5-HTCNS neuroscience & therapeutics · 2021
    Article
  17. Article
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

7 authors at 3 institutions in 1 country.

Fangfang WuDepartment of Neurology, Affiliated ZhongDa Hospital, Neuropsychiatric Institute, School of Medicine, Southeast University, Nanjing, China.ORCID 0000-0003-4033-6644
Hongbin SunSchool of Life Science and Technology, Shanghai Tech University, Shanghai, China.
Weigang GongDepartment of Neurology, Affiliated ZhongDa Hospital, Neuropsychiatric Institute, School of Medicine, Southeast University, Nanjing, China.
Xiaoli LiDepartment of Neurology, Affiliated ZhongDa Hospital, Neuropsychiatric Institute, School of Medicine, Southeast University, Nanjing, China.
Zhaohui PanDepartment of Neurology, Affiliated ZhongDa Hospital, Neuropsychiatric Institute, School of Medicine, Southeast University, Nanjing, China.
Han ShanDepartment of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, China.
Zhijun ZhangDepartment of Neurology, Affiliated ZhongDa Hospital, Neuropsychiatric Institute, School of Medicine, Southeast University, Nanjing, China.ORCID 0000-0001-5480-0888
Zhongda Hospital Southeast University · CNFudan University Shanghai Cancer Center · CNShanghaiTech University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe two-pore domain potassium channel TREK-1 is a member of background K

methodsThe expression of TREK-1 was examined in a mouse model of chronic unpredictable mild stress (CUMS) using immunoblotting. Neuron-specific genetic manipulation of TREK-1 was performed through adeno-associated virus. Behavioral tests were performed to evaluate depression-related behaviors. Electrophysiological recordings were used to evaluate synaptic plasticity. Golgi staining was used to examine neuroplasticity.

resultsTREK-1 expression was increased in the mouse hippocampus after CUMS. Knockdown of TREK-1 in hippocampal neurons significantly attenuated depressive-like behaviors and prevented the decrease of CUMS-induced synaptic proteins in mice. Further examination indicated that neuron-specific knockdown of TREK-1 in the hippocampus prevented stress-induced impairment of glutamatergic synaptic transmission in the CA1 region. Moreover, chronic TREK-1 inhibition protected against CUMS-induced depressive-like behaviors and impairment of synaptogenesis in the hippocampus.

conclusionOur results indicate a role for TREK-1 in the modulation of synaptic plasticity in a mouse model of depression. These findings will provide insight into the pathological mechanism of depression and further evidence for a novel target for antidepressant treatment.

Indexed as

AnimalsBridged Bicyclo CompoundsDepressionHippocampusMaleMiceMice, Inbred C57BLNeuronal PlasticityOxazolesPeptidesPotassium Channels, Tandem Pore DomainRNA, Small InterferingBridged Bicyclo CompoundsOxazolesPeptidespotassium channel protein TREK-1Potassium Channels, Tandem Pore DomainRNA, Small InterferingSID1900spadin peptidedepressionhippocampusmiceneuronal plasticityTREK-1

Identifiers

PMID32864894
PMCPMC7816204
OpenAlexW3082593112

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Registered trials

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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.