Evidence map›Paper›PMID 22508465›Full record

ArticleMolecular psychiatry2012

The ADHD-susceptibility gene lphn3.1 modulates dopaminergic neuron formation and locomotor activity during zebrafish development.

M Lange, W Norton, M Coolen, M Chaminade, S Merker, F Proft, A Schmitt, P Vernier, K-P Lesch, L Bally-Cuif

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 3 pooled it
6.7field-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

95 citing papers in PubMed, 3 syntheses or guidelines pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Bayesian Genome-Wide Association Study of Feed Efficiency Traits in Pigs.Animals : an open access journal from MDPI · 2026
    Article
  5. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. bioRxiv : the preprint server for biology · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Novel non-stimulants rescue hyperactive phenotype in an adgrl3.1 mutant zebrafish model of ADHD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  20. Loss ofFrontiers in neuroscience · 2023
    Article

35 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

10 authors at 4 institutions in 2 countries.

M LangeZebrafish Neurogenetics Group, Laboratory of Neurobiology and Development (N&D), CNRS UPR 3294, Institute of Neurobiology Alfred Fessard, Avenue de la Terrasse, Gif-sur-Yvette cédex, France.
W Norton
M Coolen
M Chaminade
S Merker
F Proft
A Schmitt
P Vernier
K-P Lesch
L Bally-Cuif
Laboratoire de Neurobiologie Cellulaire et Moléculaire · FRCentre National de la Recherche Scientifique · FRSocial Neuroscience Lab · DEUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, hyperactivity, increased impulsivity and emotion dysregulation. Linkage analysis followed by fine-mapping identified variation in the gene coding for Latrophilin 3 (LPHN3), a putative adhesion-G protein-coupled receptor, as a risk factor for ADHD. In order to validate the link between LPHN3 and ADHD, and to understand the function of LPHN3 in the etiology of the disease, we examined its ortholog lphn3.1 during zebrafish development. Loss of lphn3.1 function causes a reduction and misplacement of dopamine-positive neurons in the ventral diencephalon and a hyperactive/impulsive motor phenotype. The behavioral phenotype can be rescued by the ADHD treatment drugs methylphenidate and atomoxetine. Together, our results implicate decreased Lphn3 activity in eliciting ADHD-like behavior, and demonstrate its correlated contribution to the development of the brain dopaminergic circuitry.

Indexed as

AnimalsAtomoxetine HydrochlorideAttention Deficit Disorder with HyperactivityDiencephalonDisease Models, AnimalDopaminergic NeuronsDopamine Uptake InhibitorsGene Knockdown TechniquesMethylphenidateMolecular ImagingMotor ActivityNerve DegenerationPropylaminesReceptors, PeptideZebrafishalpha-latrotoxin receptorAtomoxetine HydrochlorideDopamine Uptake InhibitorsMethylphenidatePropylaminesReceptors, Peptide

Identifiers

PMID22508465
OpenAlexW1964871373

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.