Evidence map›Paper›PMID 24548786›Full record

ReviewNeuroscience and biobehavioral reviews2014

Dysregulation of group-I metabotropic glutamate (mGlu) receptor mediated signalling in disorders associated with Intellectual Disability and Autism.

Simona D'Antoni, Michela Spatuzza, Carmela M Bonaccorso, Sebastiano A Musumeci, Lucia Ciranna, Ferdinando Nicoletti, Kimberly M Huber, Maria Vincenza Catania

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience and biobehavioral reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
9.8field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. The ISR downstream effector ATF4 promotes mGluR-dependent long-term depression and associated behavior.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Narrative Review: Update on the Molecular Diagnosis of Fragile X Syndrome.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Review
  13. Altered Expression andCurrent neuropharmacology · 2022
    Article
  14. Article
  15. Review
  16. Prenatal Zinc Deficient Mice as a Model for Autism Spectrum Disorders.International journal of molecular sciences · 2022
    Review
  17. Review
  18. Review
  19. Article
  20. Loss of mGluR5 in D1 Receptor-Expressing Neurons Improves Stress Coping.International journal of molecular sciences · 2021
    Article

1 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

8 authors at 6 institutions in 2 countries.

Simona D'AntoniInstitute of Neurological Sciences, the National Research Council of Italy (CNR), Catania, Italy.
Michela SpatuzzaInstitute of Neurological Sciences, the National Research Council of Italy (CNR), Catania, Italy.
Carmela M BonaccorsoIRCCS Oasi Maria SS, Troina (EN), Italy.
Sebastiano A MusumeciIRCCS Oasi Maria SS, Troina (EN), Italy.
Lucia CirannaDepartment of Biomedical Sciences, section of Physiology, University of Catania, Italy.
Ferdinando NicolettiIRCCS Neuromed, Pozzilli (IS), Italy; University of Rome La Sapienza, Rome, Italy.
Kimberly M HuberUniversity of Texas Southwestern Medical Center, Department of Neuroscience, Dallas, TX 75390-9111, USA.
Maria Vincenza CataniaInstitute of Neurological Sciences, the National Research Council of Italy (CNR), Catania, Italy; IRCCS Oasi Maria SS, Troina (EN), Italy. Electronic address: mariavincenza.catania@cnr.it.
National Research Council · ITOasi Maria SS · ITI.R.C.C.S. Oasi Maria SS · ITIstituto Neurologico Mediterraneo · ITThe University of Texas Southwestern Medical Center · USUniversity of Catania · IT

Funding

Mechanisms of mGluR-dependent synaptic plasticityR01NS045711 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI HUBER, KIMBERLY M. · 2003 to 2015
$4.6M
NINDS NIH HHS R01 NS045711Telethon GGP13145
6 · The paper itself

Abstract

Activation of group-I metabotropic glutamate receptors, mGlu1 and mGlu5, triggers a variety of signalling pathways in neurons and glial cells, which are differently implicated in synaptic plasticity. The earliest and much of key studies discovered abnormal mGlu5 receptor function in Fragile X syndrome (FXS) mouse models which then motivated more recent work that finds mGlu5 receptor dysfunction in related disorders such as intellectual disability (ID), obsessive-compulsive disorder (OCD) and autism. Therefore, mGlu1/5 receptor dysfunction may represent a common aetiology of these complex diseases. Furthermore, many studies have focused on dysregulation of mGlu5 signalling to synaptic protein synthesis. However, emerging evidence finds abnormal mGlu5 receptor interactions with its scaffolding proteins in FXS which results in mGlu5 receptor dysfunction and phenotypes independent of signalling to protein synthesis. Finally, both an increased and reduced mGlu5 functioning seem to be associated with ID and autism spectrum disorders, with important consequences for potential treatment of these developmental disorders.

Indexed as

Signal TransductionAnimalsAutistic DisorderFragile X SyndromeHumansIntellectual DisabilityNeuronal PlasticityReceptor, Metabotropic Glutamate 5Receptors, Metabotropic Glutamatemetabotropic glutamate receptor type 1Receptor, Metabotropic Glutamate 5Receptors, Metabotropic GlutamateDevelopmental disordersFmrpFragile XHomerMental retardationNeuroliginPTENSAPAP3SHANKSynaptic plasticityTSC

Identifiers

PMID24548786
PMCPMC5499156
OpenAlexW2022138812

What OpenQuestion 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 OpenQuestion graph.