Evidence map›Paper›PMID 21766041›Full record

ReviewNeural plasticity2011

Alterations of GABAergic signaling in autism spectrum disorders.

Rocco Pizzarelli, Enrico Cherubini

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Neural plasticity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03826940 (Linking Inhibition From Molecular to Systems and Cognitive Levels), which is not on this map. Cited by 180 papers.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed
7.7field-weighted citation impact, top 1% 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.

NCT03826940 nacompletednot on this mapstarted 2019, after this paper: background citation

Linking Inhibition From Molecular to Systems and Cognitive Levels: a Preclinical and Clinical Approach in Autism Spectrum Disorders and Neurofibromatosis.

TypeinterventionalSponsorUniversity of CoimbraRan2019 to 2020Enrolled16ConditionsAutism Spectrum Disorder, Neurofibromatosis 1ArmsLovastatin 60 MG, Placebos
3 · Its place in the literature

Who cites it

180 citing papers in PubMed, 315 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Article
  8. The Microbiota in the Diagnosis and Treatment of Autism Spectrum Disorder.International journal of molecular sciences · 2026
    Review
  9. A Developmental Neuroimmune Cascade Model of Autism Spectrum Disorder.International journal of molecular sciences · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Terminal nucleotidyltransferaseRNA (New York, N.Y.) · 2025
    Article
  20. Article

120 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

2 authors at 1 institution in 1 country.

Rocco PizzarelliNeurobiology Sector and IIT Unit, International School for Advanced Studies (SISSA), Via Bonomea 265, 34136 Trieste, Italy.
Enrico Cherubini
Scuola Internazionale Superiore di Studi Avanzati · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorders (ASDs) comprise a heterogeneous group of pathological conditions, mainly of genetic origin, characterized by stereotyped behavior, marked impairment in verbal and nonverbal communication, social skills, and cognition. Interestingly, in a small number of cases, ASDs are associated with single mutations in genes encoding for neuroligin-neurexin families. These are adhesion molecules which, by regulating transsynaptic signaling, contribute to maintain a proper excitatory/inhibitory (E/I) balance at the network level. Furthermore, GABA, the main inhibitory neurotransmitter in adult life, at late embryonic/early postnatal stages has been shown to depolarize and excite targeted cell through an outwardly directed flux of chloride. The depolarizing action of GABA and associated calcium influx regulate a variety of developmental processes from cell migration and differentiation to synapse formation. Here, we summarize recent data concerning the functional role of GABA in building up and refining neuronal circuits early in development and the molecular mechanisms regulating the E/I balance. A dysfunction of the GABAergic signaling early in development leads to a severe E/I unbalance in neuronal circuits, a condition that may account for some of the behavioral deficits observed in ASD patients.

Indexed as

BrainChildChild Development Disorders, Pervasivegamma-Aminobutyric AcidHumansNeural InhibitionNeuronsSynaptic Transmissiongamma-Aminobutyric Acid

Identifiers

PMID21766041
PMCPMC3134996
OpenAlexW2127590260

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.