Evidence map›Paper›PMID 29674117›Full record

ArticleBrain stimulation

Electroconvulsive seizures influence dendritic spine morphology and BDNF expression in a neuroendocrine model of depression.

Kristen R Maynard, John W Hobbs, Sumita K Rajpurohit, Keri Martinowich

Open access · greenAbstract read
In one paragraph

Article in Brain stimulation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Effects of electroconvulsive shock on the function, circuitry, and transcriptome of dentate gyrus granule neurons.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  11. Neurogenesis-independent mechanisms of MRI-detectable hippocampal volume increase following electroconvulsive stimulation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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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

4 authors at 1 institution in 1 country.

Kristen R MaynardLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, 21205, United States.
John W HobbsLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, 21205, United States.
Sumita K RajpurohitLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, 21205, United States.
Keri MartinowichLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, MD, 21205, United States; Departments of Neuroscience, Psychiatry and Behavioral Sciences, Johns Hopkins Medical School, Baltimore, MD, 21205, United States. Electronic address: Keri.martinowich@libd.org.
Lieber Institute for Brain Development · US

Funding

Regulation of neural activity in fear circuits by promoter IV derived BDNFR01MH105592 · NIMH · LIEBER INSTITUTE, INC. · PI MARTINOWICH, KERI · 2015 to 2024
$5.6M
NIMH NIH HHS R01 MH105592
6 · The paper itself

Abstract

backgroundElectroconvulsive therapy (ECT) is a rapid and effective treatment for major depressive disorder. Chronic stress-induced depression causes dendrite atrophy and deficiencies in brain-derived neurotrophic factor (BDNF), which are reversed by anti-depressant drugs. Electroconvulsive seizures (ECS), an animal model of ECT, robustly increase BDNF expression and stimulate dendritic outgrowth.

objectiveThe present study aims to understand cellular and molecular plasticity mechanisms contributing to the efficacy of ECS following chronic stress-induced depression.

methodsWe quantify Bdnf transcript levels and dendritic spine density and morphology on cortical pyramidal neurons in mice exposed to vehicle or corticosterone and receiving either Sham or ECS treatment.

resultsECS rescues corticosterone-induced defects in spine morphology and elevates Bdnf exon 1 and exon 4-containing transcripts in cortex.

conclusionsDendritic spine remodeling and induction of activity-induced BDNF in the cortex represent important cellular and molecular plasticity mechanisms underlying the efficacy of ECS for treatment of chronic stress-induced depression.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCerebral CortexDendritic SpinesDepressionDisease Models, AnimalElectroconvulsive TherapyGene ExpressionMaleMiceSeizuresBrain-Derived Neurotrophic FactorBrain-derived neurotrophic factor (BDNF)Cingulate cortexDendritic spineECTElectroconvulsive seizuresMorphology

Identifiers

PMID29674117
PMCPMC6245665
OpenAlexW2796012918

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.