Evidence map›Paper›PMID 26899129›Full record

ArticleNeuroscience2016

Role of TrkB in the anxiolytic-like and antidepressant-like effects of vagal nerve stimulation: Comparison with desipramine.

A P Shah, F R Carreno, H Wu, Y A Chung, A Frazer

Open access · greenAbstract readComparative Study
In one paragraph

Article in Neuroscience, 2016. 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
1.8field-weighted citation impact, top 15% 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, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. The gut-brain axis and cognitive control: A role for the vagus nerve.Seminars in cell & developmental biology · 2024
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Vagal Nerve Stimulation for Treatment-Resistant Depression.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
    Review
  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

5 authors at 1 institution in 1 country.

A P ShahDepartment of Pharmacology and Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, TX, USA. Electronic address: ashah69@jhmi.edu.
F R CarrenoDepartment of Pharmacology and Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, TX, USA.
H WuDepartment of Pharmacology and Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, TX, USA.
Y A ChungDepartment of Pharmacology and Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, TX, USA.
A FrazerDepartment of Pharmacology and Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, TX, USA; South Texas Veterans Health Care System (STVHCS), Audie L. Murphy Division, San Antonio, TX, USA.
The University of Texas Health Science Center at San Antonio · US

Funding

Vagal Nerve Stimulation & Antidepressants: c-Fos, deltaFosB and TrkB ActivationR01MH082933 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FRAZER, ALAN · 2008 to 2012
$1.7M
NIMH NIH HHS MH082933NIMH NIH HHS R01 MH082933
6 · The paper itself

Abstract

A current hypothesis regarding the mechanism of antidepressant (AD) action suggests the involvement of brain-derived neurotrophic factor (BDNF). Consistent with this hypothesis, the receptor for BDNF (and neurotrophin 4/5 (NT-4/5)), Tropomyosin-related kinase B (TrkB), is activated in rodents by treatment with classical AD drugs. Vagal nerve stimulation (VNS), a therapy for treatment resistant depression (TRD), also activates TrkB in rodents. However, the role of this receptor in the therapeutic effects of VNS is unclear. In the current study, the involvement of TrkB in the effects of VNS was investigated in rats using its inhibitor, K252a. Anxiolytic-like and AD-like effects were analyzed using the novelty suppressed feeding test (NSFT) and forced swim test (FST), respectively. K252a blocked the anxiolytic-like effect of chronic VNS treatment and the AD-like effect of acute VNS treatment. By contrast, blocking TrkB did not prevent either the anxiolytic-like or AD-like effect of chronic treatment with desipramine (DMI), a selective noradrenergic reuptake inhibitor; it did, however, block the acute effect of DMI in the FST. To examine whether the activation of TrkB caused by either VNS or DMI is ligand-dependent, use was made of TrkB-Fc, a molecular scavenger for ligands of TrkB. Intraventricular administration of TrkB-Fc blocked the acute activation of TrkB induced by either treatment, indicating that treatment-induced activation of this receptor is ligand-dependent. The behavioral results highlight differences in the involvement of TrkB in the chronic effects of an AD drug and a stimulation therapy as well as its role in acute versus chronic effects of DMI.

Indexed as

Vagus Nerve StimulationAdrenergic Uptake InhibitorsAnimalsAnti-Anxiety AgentsAntidepressive Agents, TricyclicAnxiety DisordersCarbazolesDepressive DisorderDesipramineDisease Models, AnimalEnzyme InhibitorsIndole AlkaloidsMaleMotor ActivityPhosphorylationRats, Sprague-DawleyAdrenergic Uptake InhibitorsAnti-Anxiety AgentsAntidepressive Agents, TricyclicCarbazolesDesipramineEnzyme InhibitorsIndole AlkaloidsReceptor, trkBstaurosporine aglyconeantidepressantsBDNFdepressiondesipramineTrkBvagal nerve stimulation

Identifiers

PMID26899129
PMCPMC4817548
OpenAlexW2278902808

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.