Evidence map›Paper›PMID 24904277›Full record

ReviewFrontiers in cellular neuroscience2014

Modulation of GABAergic transmission in development and neurodevelopmental disorders: investigating physiology and pathology to gain therapeutic perspectives.

Gabriele Deidda, Ignacio F Bozarth, Laura Cancedda

2 registry-linked trialsOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
11.7field-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.

NCT06228872 naunknown statusnot on this mapstarted 2024, after this paper: background citation

Direct Current Transcranial Stimulation as Cognitive Rehabilitation Therapy in Post-Traumatic Brain Injury Patients.

TypeinterventionalSponsorMutual de Seguridad Hospital ClinicoRan2024 to 2025Enrolled38ConditionsTraumatic Brain Injury, Cognitive ImpairmentArmsCognitive Computerized Training (CCT) plus Anodic transcranial Direct Current Stimulation (tDCS), Cognitive Computerized Training (CCT) plus sham transcranial Direct Current Stimulation (tDCS)
NCT06465823 phase2recruitingnot on this mapstarted 2023, after this paper: background citation

A Phase 2 Double Blind Placebo Controlled Study on the Efficacy of Bumetanide for Cognitive Improvement in Children and Adolescents With Down Syndrome

TypeinterventionalSponsorStefano VicariRan2023 to 2026Enrolled64ConditionsDown SyndromeArmsBumetanide, Placebo
3 · Its place in the literature

Who cites it

103 citing papers in PubMed, 191 citations in OpenAlex.

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  17. GABAProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. GABA system as the cause and effect in early development.Neuroscience and biobehavioral reviews · 2024
    Review
  19. Article
  20. Article

43 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

3 authors at 1 institution in 1 country.

Gabriele DeiddaDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia Genova, Italy.
Ignacio F BozarthDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia Genova, Italy.
Laura CanceddaDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia Genova, Italy.
Italian Institute of Technology · IT

Funding

Telethon GGP10135Telethon GGP13187
6 · The paper itself

Abstract

During mammalian ontogenesis, the neurotransmitter GABA is a fundamental regulator of neuronal networks. In neuronal development, GABAergic signaling regulates neural proliferation, migration, differentiation, and neuronal-network wiring. In the adult, GABA orchestrates the activity of different neuronal cell-types largely interconnected, by powerfully modulating synaptic activity. GABA exerts these functions by binding to chloride-permeable ionotropic GABAA receptors and metabotropic GABAB receptors. According to its functional importance during development, GABA is implicated in a number of neurodevelopmental disorders such as autism, Fragile X, Rett syndrome, Down syndrome, schizophrenia, Tourette's syndrome and neurofibromatosis. The strength and polarity of GABAergic transmission is continuously modulated during physiological, but also pathological conditions. For GABAergic transmission through GABAA receptors, strength regulation is achieved by different mechanisms such as modulation of GABAA receptors themselves, variation of intracellular chloride concentration, and alteration in GABA metabolism. In the never-ending effort to find possible treatments for GABA-related neurological diseases, of great importance would be modulating GABAergic transmission in a safe and possibly physiological way, without the dangers of either silencing network activity or causing epileptic seizures. In this review, we will discuss the different ways to modulate GABAergic transmission normally at work both during physiological and pathological conditions. Our aim is to highlight new research perspectives for therapeutic treatments that reinstate natural and physiological brain functions in neuro-pathological conditions.

Indexed as

cation chloride cotransportersGABAGABAA receptorGABA metabolismneurodevelopmental disorders

Identifiers

PMID24904277
PMCPMC4033255
OpenAlexW2104834189

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.