Evidence map›Paper›PMID 21893166›Full record

ArticleNeuroscience2011

Natural and engineered coding variation in antidepressant-sensitive serotonin transporters.

R Ye, R D Blakely

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Essential Contributions of Serotonin Transporter Inhibition to the Acute and Chronic Actions of Fluoxetine and Citalopram in the SERT Met172 Mouse.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Common and rare alleles of the serotonin transporter gene, SLC6A4, associated with Tourette's disorder.Movement disorders : official journal of the Movement Disorder Society · 2013
    Article
  15. Review
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 1 institution in 1 country.

R YeDepartment of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232-8548, USA.
R D Blakely
Vanderbilt University · US

Funding

Project 6 Interactions of Serotonin and Circadian Signaling NetworksP50MH078028 · NIMH · VANDERBILT UNIVERSITY · PI BLAKELY, RANDY D. · 2007 to 2011
$9.8M
Regulation of Serotonin TransportersR01MH094527 · NIMH · VANDERBILT UNIVERSITY · PI BLAKELY, RANDY D. · 2011 to 2021
$4.4M
REGULATION OF SEROTONIN TRANSPORTERSR01DA007390 · NIDA · VANDERBILT UNIVERSITY · PI BLAKELY, RANDY D. · 1991 to 2010
$3.9M
Transgenic Mouse Model to Address Heterogeneity in Autism Spectrum DisordersR01HD065278 · NICHD · VANDERBILT UNIVERSITY · PI BLAKELY, RANDY D. · 2009 to 2010
$923k
NICHD NIH HHS HD065278NICHD NIH HHS R01 HD065278NIDA NIH HHS R01 DA007390NIMH NIH HHS MH094527NIMH NIH HHS P50 MH078028NIMH NIH HHS P50MH078028NIMH NIH HHS R01 MH094527
6 · The paper itself

Abstract

The presynaptic serotonin (5-HT) transporter (SERT) is a key regulator of 5-HT signaling and is a major target for antidepressant medications and psychostimulants. In recent years, studies of natural and engineered genetic variation in SERT have provided new opportunities to understand structural dimensions of drug interactions and regulation of the transporter, to explore 5-HT contributions to antidepressant action, and to assess the impact of SERT-mediated 5-HT contributions to neuropsychiatric disorders. Here we review three examples from our recent studies where genetic changes in SERT, identified or engineered, have led to new models, findings, and theories that cast light on new dimensions of 5-HT action in the CNS and periphery. First, we review our work to identify specific residues through which SERT recognizes antagonists, and the conversion of this knowledge to the creation of mice lacking high-affinity antidepressant and cocaine sensitivity. Second, we discuss our studies of functional coding variation in SERT that exists in commonly used strains of inbred mice, and how this variation is beginning to reveal novel 5-HT-associated phenotypes. Third, we review our identification and functional characterization of multiple, hyperactive SERT coding variants in subjects with autism. Each of these activities has driven the development of new model systems that can be further exploited to understand the contribution of 5-HT signaling to risk for neuropsychiatric disorders and their treatment.

Indexed as

AnimalsAntidepressive AgentsAutistic DisorderBrainHumansMiceMice, TransgenicSerotoninSerotonin Plasma Membrane Transport ProteinsAntidepressive AgentsSerotoninSerotonin Plasma Membrane Transport Proteins

Identifiers

PMID21893166
PMCPMC3850749
OpenAlexW1978465685

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.