Evidence map›Paper›PMID 25136890›Full record

ArticleTranslational psychiatry2014

Dysfunctional dopaminergic neurotransmission in asocial BTBR mice.

M Squillace, L Dodero, M Federici, S Migliarini, F Errico, F Napolitano, P Krashia, A Di Maio, A Galbusera, A Bifone and 5 more

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 72 citations in OpenAlex.

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  14. Altered Expression andCurrent neuropharmacology · 2022
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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

15 authors at 6 institutions in 1 country.

M SquillaceCeinge Biotecnologie Avanzate, Naples, Italy.
L Dodero1] Istituto Italiano di Tecnologia, Center for Neuroscience and Cognitive Systems, Rovereto, Italy [2] Istituto Italiano di Tecnologia, Pavis, Genoa, Italy.
M Federici1] Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy [2] Laboratorio di Neurologia Sperimentale, IRCCS Fondazione Santa Lucia, Rome, Italy.
S MigliariniDepartment of Biology, Unit of Cell and Developmental Biology, University of Pisa, Pisa, Italy.
F Errico1] Ceinge Biotecnologie Avanzate, Naples, Italy [2] Department of Molecular Medicine and Medical Biotechnology, University of Naples 'Federico II', Naples, Italy.
F Napolitano1] Ceinge Biotecnologie Avanzate, Naples, Italy [2] Department of Molecular Medicine and Medical Biotechnology, University of Naples 'Federico II', Naples, Italy.
P KrashiaDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.
A Di MaioCeinge Biotecnologie Avanzate, Naples, Italy.
A GalbuseraIstituto Italiano di Tecnologia, Center for Neuroscience and Cognitive Systems, Rovereto, Italy.
A BifoneIstituto Italiano di Tecnologia, Center for Neuroscience and Cognitive Systems, Rovereto, Italy.
M L ScattoniNeurotoxicology and Neuroendocrinology Section, Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy.
M PasqualettiDepartment of Biology, Unit of Cell and Developmental Biology, University of Pisa, Pisa, Italy.
N B Mercuri1] Department of Systems Medicine, University of Rome Tor Vergata, Rome, Italy [2] Laboratorio di Neurologia Sperimentale, IRCCS Fondazione Santa Lucia, Rome, Italy.
A Usiello1] Ceinge Biotecnologie Avanzate, Naples, Italy [2] Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, Second University of Naples (SUN), Caserta, Italy.
A GozziIstituto Italiano di Tecnologia, Center for Neuroscience and Cognitive Systems, Rovereto, Italy.
Ceinge Biotecnologie Avanzate (Italy) · ITCenter for Neuroscience and Cognitive Systems · ITUniversity of Pisa · ITIstituto Superiore di Sanità · ITItalian Institute of Technology · ITUniversity of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorders (ASD) are neurodevelopmental conditions characterized by pronounced social and communication deficits and stereotyped behaviours. Recent psychosocial and neuroimaging studies have highlighted reward-processing deficits and reduced dopamine (DA) mesolimbic circuit reactivity in ASD patients. However, the neurobiological and molecular determinants of these deficits remain undetermined. Mouse models recapitulating ASD-like phenotypes could help generate hypotheses about the origin and neurophysiological underpinnings of clinically relevant traits. Here we used functional magnetic resonance imaging (fMRI), behavioural and molecular readouts to probe dopamine neurotransmission responsivity in BTBR T(+) Itpr3(tf)/J mice (BTBR), an inbred mouse line widely used to model ASD-like symptoms owing to its robust social and communication deficits, and high level of repetitive stereotyped behaviours. C57BL/6J (B6) mice were used as normosocial reference comparators. DA reuptake inhibition with GBR 12909 produced significant striatal DA release in both strains, but failed to elicit fMRI activation in widespread forebrain areas of BTBR mice, including mesolimbic reward and striatal terminals. In addition, BTBR mice exhibited no appreciable motor responses to GBR 12909. DA D1 receptor-dependent behavioural and signalling responses were found to be unaltered in BTBR mice, whereas dramatic reductions in pre- and postsynaptic DA D2 and adenosine A2A receptor function was observed in these animals. Overall these results document profoundly compromised DA D2-mediated neurotransmission in BTBR mice, a finding that is likely to have a role in the distinctive social and behavioural deficits exhibited by these mice. Our results call for a deeper investigation of the role of dopaminergic dysfunction in mouse lines exhibiting ASD-like phenotypes, and possibly in ASD patient populations.

Indexed as

Disease Models, AnimalAnimalsArousalBehavior, AnimalChild Development Disorders, PervasiveDopamineLimbic SystemMagnetic Resonance ImagingMesencephalonMiceMice, Inbred C57BLMice, Inbred StrainsNerve NetReceptors, Dopamine D2Reference ValuesSocial BehaviorDopamineReceptors, Dopamine D2

Identifiers

PMID25136890
PMCPMC4150243
OpenAlexW2071488844

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.