Evidence map›Paper›PMID 25823514›Full record

ReviewMolecular neurobiology2016

Revisiting the Serotonin Hypothesis: Implications for Major Depressive Disorders.

Marc Fakhoury

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 4 pooled it
5.7field-weighted citation impact, top 3% 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

100 citing papers in PubMed, 4 syntheses or guidelines pooled it, 242 citations in OpenAlex.

  1. Microbiome and well-being: a meta-analysis.NPJ biofilms and microbiomes · 2025
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Decreased Pretreatment Amygdalae Serotonin Transporter Binding in Unipolar Depression Remitters: A Prospective PET Study.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2018
    Trial
  6. Article
  7. Article
  8. Article
  9. Review
  10. Do sex and gender matter in the pharmacological treatment of depression?Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  11. Gender Differences and Comorbidities in Major Depression.Advances in experimental medicine and biology · 2026
    Review
  12. Review
  13. Neuroprotective Effects of Glucosamine in Huntington's Disease Through NLRP3 Inflammasome Inhibition.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Feasibility of Using Serum, Plasma, and Platelet 5-hydroxytryptamine as Peripheral Biomarker for the Depression Diagnosis and Response Evaluation to Antidepressants: Animal Experimental Study.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2024
    Article
  19. Article
  20. Review

40 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

1 author at 1 institution in 1 country.

Marc FakhouryDepartment of Neuroscience, Faculty of Medicine, University of Montreal, Montreal, QC, H3C3J7, Canada. marc.fakhoury@umontreal.ca.
Université de Montréal · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Major depressive disorder (MDD) is a heritable neuropsychiatric disease associated with severe changes at cellular and molecular levels. Its diagnosis mainly relies on the characterization of a wide range of symptoms including changes in mood and behavior. Despite the availability of antidepressant drugs, 10 to 30 % of patients fail to respond after a single or multiple treatments, and the recurrence of depression among responsive patients is very high. Evidence from the past decades suggests that the brain neurotransmitter serotonin (5-HT) is incriminated in MDD, and that a dysfunction of 5-HT receptors may play a role in the genesis of this disease. The 5-HT membrane transporter protein (SERT), which helps regulate the serotonergic transmission, is also implicated in MDD and is one of the main targets of antidepressant therapy. Although a number of behavioral tests and animal models have been developed to study depression, little is known about the neurobiological bases of MDD. Understanding the role of the serotonergic pathway will significantly help improve our knowledge of the pathophysiology of depression and may open up avenues for the development of new antidepressant drugs. The overarching goal of this review is to present recent findings from studies examining the serotonergic pathway in MDD, with a focus on SERT and the serotonin 1A (5-HT1A), serotonin 1B (5-HT1B), and serotonin 2A (5-HT2A) receptors. This paper also describes some of the main molecules involved in the internalization of 5-HT receptors and illustrates the changes in 5-HT neurotransmission in knockout mice and animal model of depression.

Indexed as

Models, BiologicalAnimalsAntidepressive AgentsDisease Models, AnimalEndocytosisHumansMajor Depressive DisorderSerotoninAntidepressive AgentsSerotoninGene knockoutG-protein couplingMajor depressive disorderSerotoninSerotonin receptorTransporter

Identifiers

PMID25823514
OpenAlexW2031775832

What OpenQuestion holds

Textmetadata
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.