Evidence map›Paper›PMID 21766043›Full record

ReviewNeural plasticity2011

Functional consequences of the disturbances in the GABA-mediated inhibition induced by injuries in the cerebral cortex.

Barbara Imbrosci, Thomas Mittmann

Abstract 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. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–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

22 citing papers in PubMed.

  1. The aging motor system as a model for plastic changes of GABA-mediated intracortical inhibition and their behavioral relevance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Trial
  2. Differential Roles of Neuro-Inflammatory Regulator, MAPK11 in Cortex and Hippocampus Following Post-Stroke Cognitive Impairments in Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  3. Review
  4. GABAInternational journal of molecular sciences · 2022
    Article
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  14. Review
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  18. Synaptic plasticity and PDGF signaling defects underlie clinical progression in multiple sclerosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
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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

2 authors.

Barbara ImbrosciInstitute of Physiology and Pathophysiology, Medical Center of the Johannes Gutenberg University, Duesbergweg 6, 55128 Mainz, Germany. imbrosci@uni-mainz.de
Thomas Mittmann

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cortical injuries are often reported to induce a suppression of the intracortical GABAergic inhibition in the surviving, neighbouring neuronal networks. Since GABAergic transmission provides the main source of inhibition in the mammalian brain, this condition may lead to hyperexcitability and epileptiform activity of cortical networks. However, inhibition plays also a crucial role in limiting the plastic properties of neuronal circuits, and as a consequence, interventions aiming to reestablish a normal level of inhibition might constrain the plastic capacity of the cortical tissue. A promising strategy to minimize the deleterious consequences of a modified inhibitory transmission without preventing the potential beneficial effects on cortical plasticity may be to unravel distinct GABAergic signaling pathways separately mediating these positive and negative events. Here, gathering data from several recent studies, we provide new insights to better face with this "double coin" condition in the attempt to optimize the functional recovery of patients.

Indexed as

Brain InjuriesCerebral Cortexgamma-Aminobutyric AcidHumansNeural InhibitionNeuronsSynaptic Transmissiongamma-Aminobutyric Acid

Identifiers

PMID21766043
PMCPMC3135051

What OpenQuestion holds

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Registered trials

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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.