Evidence map›Paper›PMID 31492942›Full record

ArticleMolecular psychiatry2021

The epistatic interaction between the dopamine D3 receptor and dysbindin-1 modulates higher-order cognitive functions in mice and humans.

G M Leggio, S A Torrisi, R Mastrogiacomo, D Mauro, M Chisari, C Devroye, D Scheggia, M Nigro, F Geraci, N Pintori and 12 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Probing the Skin-Brain Axis: New Vistas Using Mouse Models.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

22 authors.

G M LeggioDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy. gianmarco.leggio@unict.it.
S A TorrisiDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
R MastrogiacomoDepartment of Neuroscience and Brain Technologies, Genetics of Cognition laboratory, Istituto Italiano di Tecnologia, via Morego, 30, 16163, Genova, Italy.
D MauroDepartment of Neuroscience and Brain Technologies, Genetics of Cognition laboratory, Istituto Italiano di Tecnologia, via Morego, 30, 16163, Genova, Italy.
M ChisariDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
C DevroyeDepartment of Neuroscience and Brain Technologies, Genetics of Cognition laboratory, Istituto Italiano di Tecnologia, via Morego, 30, 16163, Genova, Italy.
D ScheggiaDepartment of Neuroscience and Brain Technologies, Genetics of Cognition laboratory, Istituto Italiano di Tecnologia, via Morego, 30, 16163, Genova, Italy.ORCID http://orcid.org/0000-0003-2586-9717
M NigroDepartment of Neuroscience and Brain Technologies, Genetics of Cognition laboratory, Istituto Italiano di Tecnologia, via Morego, 30, 16163, Genova, Italy.
F GeraciDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
N PintoriDepartment of Biomedical Sciences, University of Cagliari, Cagliari, Italy.
G GiurdanellaDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
L CostaDepartment of Clinical and Experimental Medicine, University of Messina, Messina, Italy.ORCID http://orcid.org/0000-0002-2465-8080
C BucoloDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
V FerrettiDepartment of Neuroscience and Brain Technologies, Genetics of Cognition laboratory, Istituto Italiano di Tecnologia, via Morego, 30, 16163, Genova, Italy.
M A SortinoDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
L CirannaDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.ORCID http://orcid.org/0000-0003-0274-6095
M A De LucaDepartment of Clinical and Experimental Medicine, University of Messina, Messina, Italy.
M MereuDepartment of Neuroscience and Brain Technologies, Genetics of Cognition laboratory, Istituto Italiano di Tecnologia, via Morego, 30, 16163, Genova, Italy.
F ManagòDepartment of Neuroscience and Brain Technologies, Genetics of Cognition laboratory, Istituto Italiano di Tecnologia, via Morego, 30, 16163, Genova, Italy.
S SalomoneDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
F DragoDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
F PapaleoDepartment of Neuroscience and Brain Technologies, Genetics of Cognition laboratory, Istituto Italiano di Tecnologia, via Morego, 30, 16163, Genova, Italy. francesco.papaleo@iit.it.ORCID http://orcid.org/0000-0002-6326-0657

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dopamine D2 and D3 receptors are implicated in schizophrenia and its pharmacological treatments. These receptors undergo intracellular trafficking processes that are modulated by dysbindin-1 (Dys). Indeed, Dys variants alter cognitive responses to antipsychotic drugs through D2-mediated mechanisms. However, the mechanism by which Dys might selectively interfere with the D3 receptor subtype is unknown. Here, we revealed an interaction between functional genetic variants altering Dys and D3. Specifically, both in patients with schizophrenia and in genetically modified mice, concomitant reduction in D3 and Dys functionality was associated with improved executive and working memory abilities. This D3/Dys interaction produced a D2/D3 imbalance favoring increased D2 signaling in the prefrontal cortex (PFC) but not in the striatum. No epistatic effects on the clinical positive and negative syndrome scale (PANSS) scores were evident, while only marginal effects on sensorimotor gating, locomotor functions, and social behavior were observed in mice. This genetic interaction between D3 and Dys suggests the D2/D3 imbalance in the PFC as a target for patient stratification and procognitive treatments in schizophrenia.

Indexed as

DysbindinReceptors, Dopamine D3SchizophreniaAnimalsCognitionHumansMiceReceptors, Dopamine D2DysbindinReceptors, Dopamine D2Receptors, Dopamine D3

Identifiers

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.