Evidence map›Paper›PMID 25787955›Full record

ArticleJournal of neurophysiology2015

Robust presynaptic serotonin 5-HT(1B) receptor inhibition of the striatonigral output and its sensitization by chronic fluoxetine treatment.

Shengyuan Ding, Li Li, Fu-Ming Zhou

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Dopamine's secret agent: serotonin.Trends in neurosciences · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Serotonergic targets for the treatment of L-DOPA-induced dyskinesia.Journal of neural transmission (Vienna, Austria : 1996) · 2018
    Review
  10. The 5-HTPsychopharmacology · 2018
    Review
  11. Article
  12. Review
  13. Article
  14. Opposing roles for serotonin in cholinergic neurons of the ventral and dorsal striatum.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
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 1 institution in 1 country.

Shengyuan DingDepartment of Pharmacology, University of Tennessee College of Medicine, Memphis, Tennessee.
Li LiDepartment of Pharmacology, University of Tennessee College of Medicine, Memphis, Tennessee.
Fu-Ming ZhouDepartment of Pharmacology, University of Tennessee College of Medicine, Memphis, Tennessee fzhou3@uthsc.edu.
University of Tennessee Health Science Center · US

Funding

Regulation of basal ganglia output neuronsR01NS058850 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ZHOU, FU-MING · 2008 to 2012
$1.3M
NINDS NIH HHS R01NS058850
6 · The paper itself

Abstract

The striatonigral projection is a striatal output pathway critical to motor control, cognition, and emotion regulation. Its axon terminals in the substantia nigra pars reticulata (SNr) express a high level of serotonin (5-HT) type 1B receptors (5-HT(1B)Rs), whereas the SNr also receives an intense 5-HT innervation that expresses 5-HT transporters, providing an anatomic substrate for 5-HT and selective 5-HT reuptake inhibitor (SSRI)-based antidepressant treatment to regulate the striatonigral output. In this article we show that 5-HT, by activating presynaptic 5-HT(1B)Rs on the striatonigral axon terminals, potently inhibited the striatonigral GABA output, as reflected in the reduction of the striatonigral inhibitory postsynaptic currents in SNr GABA neurons. Functionally, 5-HT(1B)R agonism reduced the striatonigral GABA output-induced pause of the spontaneous high-frequency firing in SNr GABA neurons. Equally important, chronic SSRI treatment with fluoxetine enhanced this presynaptic 5-HT(1B)R-mediated pause reduction in SNr GABA neurons. Taken together, these results indicate that activation of the 5-HT(1B)Rs on the striatonigral axon terminals can limit the motor-promoting GABA output. Furthermore, in contrast to the desensitization of 5-HT1 autoreceptors, chronic SSRI-based antidepressant treatment sensitizes this presynaptic 5-HT(1B)R-mediated effect in the SNr, a novel cellular mechanism that alters the striatonigral information transfer, potentially contributing to the behavioral effects of chronic SSRI treatment.

Indexed as

AnimalsAnimals, NewbornCorpus StriatumFemaleFluoxetineGABAergic NeuronsInhibitory Postsynaptic PotentialsIn Vitro TechniquesMaleMiceMice, Inbred C57BLPresynaptic TerminalsReceptor, Serotonin, 5-HT1BSelective Serotonin Reuptake InhibitorsSerotoninSerotonin AgentsFluoxetineReceptor, Serotonin, 5-HT1BSelective Serotonin Reuptake InhibitorsSerotoninSerotonin AgentsSerotonin Plasma Membrane Transport Proteins5-HT1B receptor sensitizationbasal gangliamedium spiny neuronselective serotonin reuptake inhibitorsubstantia nigra pars reticulata

Identifiers

PMID25787955
PMCPMC4455558
OpenAlexW2052016589

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.