Evidence map›Paper›PMID 26519901›Full record

ReviewNeuropharmacology2016

BDNF - a key transducer of antidepressant effects.

Carl Björkholm, Lisa M Monteggia

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 474 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
474citing papers in PubMed, 4 pooled it
19.4field-weighted citation impact, top 1% 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

474 citing papers in PubMed, 4 syntheses or guidelines pooled it, 925 citations in OpenAlex.

  1. Pooled it
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  11. Article
  12. The role of BDNF promoter VI in mediating protective effects of prophylactic (R,S)-ketamine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  13. AiScience · 2026
    Article
  14. Article
  15. Article
  16. Review
  17. 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
    Article
  18. Review
  19. Article
  20. Review

414 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Carl BjörkholmDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Lisa M MonteggiaDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: lisa.monteggia@utsouthwestern.edu.
Karolinska Institutet · SESouthwestern Medical Center · US

Funding

ANTIDEPRESSANTS & INTRACELLULAR SIGNALING LINKED TO BDNFR01MH070727 · NIMH · VANDERBILT UNIVERSITY · PI LISA M MONTEGGIA · 2005 to 2026
$8.9M
NIMH NIH HHS MH070727NIMH NIH HHS R01 MH070727
6 · The paper itself

Abstract

How do antidepressants elicit an antidepressant response? Here, we review accumulating evidence that the neurotrophin brain-derived neurotrophic factor (BDNF) serves as a transducer, acting as the link between the antidepressant drug and the neuroplastic changes that result in the improvement of the depressive symptoms. Over the last decade several studies have consistently highlighted BDNF as a key player in antidepressant action. An increase in hippocampal and cortical expression of BDNF mRNA parallels the antidepressant-like response of conventional antidepressants such as SSRIs. Subsequent studies showed that a single bilateral infusion of BDNF into the ventricles or directly into the hippocampus is sufficient to induce a relatively rapid and sustained antidepressant-like effect. Importantly, the antidepressant-like response to conventional antidepressants is attenuated in mice where the BDNF signaling has been disrupted by genetic manipulations. Low dose ketamine, which has been found to induce a rapid antidepressant effect in patients with treatment-resistant depression, is also dependent on increased BDNF signaling. Ketamine transiently increases BDNF translation in hippocampus, leading to enhanced synaptic plasticity and synaptic strength. Ketamine has been shown to increase BDNF translation by blocking NMDA receptor activity at rest, thereby inhibiting calcium influx and subsequently halting eukaryotic elongation factor 2 (eEF2) kinase leading to a desuppression of protein translation, including BDNF translation. The antidepressant-like response of ketamine is abolished in BDNF and TrkB conditional knockout mice, eEF2 kinase knockout mice, in mice carrying the BDNF met/met allele, and by intra-cortical infusions of BDNF-neutralizing antibodies. In summary, current data suggests that conventional antidepressants and ketamine mediate their antidepressant-like effects by increasing BDNF in forebrain regions, in particular the hippocampus, making BDNF an essential determinant of antidepressant efficacy.

Indexed as

AnimalsAntidepressive AgentsBrain-Derived Neurotrophic FactorDepressionDisease Models, AnimalHippocampusHumansMiceAntidepressive AgentsBrain-Derived Neurotrophic FactorBehaviorBrain-derived neurotrophic factorDepressionHippocampusSynaptic plasticity

Identifiers

PMID26519901
PMCPMC4763983
OpenAlexW1877874306

What Socratic 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 Socratic graph.