Evidence map›Paper›PMID 19428959›Full record

ReviewProgress in neurobiology2009

5-HT(1A) receptor function in major depressive disorder.

Jonathan Savitz, Irwin Lucki, Wayne C Drevets

Open access · greenAbstract readReview
In one paragraph

Review in Progress in neurobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 230 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
230citing papers in PubMed, 3 pooled it
19.2field-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

230 citing papers in PubMed, 3 syntheses or guidelines pooled it, 566 citations in OpenAlex.

  1. Pooled it
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  4. Trial
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  10. Varivax (IBRO neuroscience reports · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Pathophysiology and Treatment Strategies for Different Types of Depression.Advances in experimental medicine and biology · 2026
    Review
  17. The Complex Role of Serotonin-Dopamine-Glutamate Receptors in Major Depression.Advances in experimental medicine and biology · 2026
    Review
  18. Review
  19. Article
  20. Review

170 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

3 authors at 2 institutions in 1 country.

Jonathan SavitzSection on Neuroimaging in Mood and Anxiety Disorders, Mood and Anxiety Disorders Program, NIH/NIMH, Bethesda, MD 20892, United States. savitzj@mail.nih.gov
Irwin Lucki
Wayne C Drevets
National Institute of Mental Health · USUniversity of Pennsylvania · US

Funding

Serotonin Function and Receptor Imaging In Mood and Anxiety DisordersZIAMH002788 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI DREVETS, WAYNE C · 2009 to 2009
$392k
Intramural NIH HHS Z99 MH999999
6 · The paper itself

Abstract

Dysfunction of the serotonin 1A receptor (5-HT(1A)) may play a role in the genesis of major depressive disorder (MDD). Here we review the pharmacological, post-mortem, positron emission tomography (PET), and genetic evidence in support of this statement. We also touch briefly on two MDD-associated phenotypes, cognitive impairment and somatic pain. The results of pharmacological challenge studies with 5-HT(1A) receptor agonists are indicative of blunted endocrine responses in depressed patients. Lithium, valproate, selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), and other treatment, such as electroconvulsive shock therapy (ECT), all increase post-synaptic 5-HT(1A) receptor signaling through either direct or indirect effects. Reduced somatodendritic and postsynaptic 5-HT(1A) receptor numbers or affinity have been reported in some post-mortem studies of suicide victims, a result consistent with well-replicated PET analyses demonstrating reduced 5-HT(1A) receptor binding potential in diverse regions such as the dorsal raphe, medial prefrontal cortex (mPFC), amygdala and hippocampus. 5-HT(1A) receptor knockout (KO) mice display increased anxiety-related behavior, which, unlike in their wild-type counterparts, cannot be rescued with antidepressant drug (AD) treatment. In humans, the G allele of a single nucleotide polymorphism (SNP) in the 5-HT(1A) receptor gene (HTR1A; rs6295), which abrogates a transcription factor binding site for deformed epidermal autoregulatory factor-1 (Deaf-1) and Hes5, has been reported to be over-represented in MDD cases. Conversely, the C allele has been associated with better response to AD drugs. We raise the possibility that 5-HT(1A) receptor dysfunction represents one potential mechanism underpinning MDD and other stress-related disorders.

Indexed as

AnimalsHumansMajor Depressive DisorderReceptor, Serotonin, 5-HT1AReceptor, Serotonin, 5-HT1A

Identifiers

PMID19428959
PMCPMC2736801
OpenAlexW2130423340

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.