Evidence map›Paper›PMID 21802488›Full record

ReviewProgress in neurobiology2011

GABAergic synchronization in the limbic system and its role in the generation of epileptiform activity.

Massimo Avoli, Marco de Curtis

Open access · greenAbstract readReview
In one paragraph

Review in Progress in neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
5.8field-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

122 citing papers in PubMed, 258 citations in OpenAlex.

  1. Review
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  3. Nutrients · 2026
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62 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 2 institutions in 2 countries.

Massimo AvoliMontreal Neurological Institute and Departments of Neurology & Neurosurgery, and of Physiology, McGill University, Montreal H3A 2B4 Quebec, Canada. massimo.avoli@mcgill.ca
Marco de Curtis
Italian Institute of Technology · ITMcGill University · CA

Funding

CIHR 8109-6
6 · The paper itself

Abstract

GABA is the main inhibitory neurotransmitter in the adult forebrain, where it activates ionotropic type A and metabotropic type B receptors. Early studies have shown that GABA(A) receptor-mediated inhibition controls neuronal excitability and thus the occurrence of seizures. However, more complex, and at times unexpected, mechanisms of GABAergic signaling have been identified during epileptiform discharges over the last few years. Here, we will review experimental data that point at the paradoxical role played by GABA(A) receptor-mediated mechanisms in synchronizing neuronal networks, and in particular those of limbic structures such as the hippocampus, the entorhinal and perirhinal cortices, or the amygdala. After having summarized the fundamental characteristics of GABA(A) receptor-mediated mechanisms, we will analyze their role in the generation of network oscillations and their contribution to epileptiform synchronization. Whether and how GABA(A) receptors influence the interaction between limbic networks leading to ictogenesis will be also reviewed. Finally, we will consider the role of altered inhibition in the human epileptic brain along with the ability of GABA(A) receptor-mediated conductances to generate synchronous depolarizing events that may lead to ictogenesis in human epileptic disorders as well.

Indexed as

Cortical SynchronizationAnimalsEpilepsyGABAergic Neuronsgamma-Aminobutyric AcidHumansLimbic SystemNerve Tissue ProteinsReceptors, GABAgamma-Aminobutyric AcidNerve Tissue ProteinsReceptors, GABA

Identifiers

PMID21802488
PMCPMC4878907
OpenAlexW2125616660

What OpenQuestion holds

Textmetadata
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.