Evidence map›Paper›PMID 33826070›Full record

ReviewMolecular neurobiology2021

GABAergic Mechanisms Can Redress the Tilted Balance between Excitation and Inhibition in Damaged Spinal Networks.

Graciela Lujan Mazzone, Atiyeh Mohammadshirazi, Jorge Benjamin Aquino, Andrea Nistri, Giuliano Taccola

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

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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

5 authors at 2 institutions in 2 countries.

Graciela Lujan MazzoneInstituto de Medicina Traslacional (IIMT), CONICET-Universidad Austral, Av. Juan Domingo Perón 1500, B1629AHJ, Pilar, Argentina.ORCID https://orcid.org/0000-0003-3360-9931
Atiyeh MohammadshiraziNeuroscience Department, International School for Advanced Studies (SISSA), Via Bonomea 265, 34136, Trieste, Italy.
Jorge Benjamin AquinoInstituto de Medicina Traslacional (IIMT), CONICET-Universidad Austral, Av. Juan Domingo Perón 1500, B1629AHJ, Pilar, Argentina.ORCID https://orcid.org/0000-0002-3818-5181
Andrea NistriNeuroscience Department, International School for Advanced Studies (SISSA), Via Bonomea 265, 34136, Trieste, Italy.ORCID https://orcid.org/0000-0002-0638-0900
Giuliano TaccolaNeuroscience Department, International School for Advanced Studies (SISSA), Via Bonomea 265, 34136, Trieste, Italy. taccola@sissa.it.ORCID http://orcid.org/0000-0003-2675-1438
Scuola Internazionale Superiore di Studi Avanzati · ITConsejo Nacional de Investigaciones Científicas y Técnicas · AR

Funding

Abdus Salam International Centre for Theoretical Physics Regular Associate SchemeSISSA intramural SISSA grant
6 · The paper itself

Abstract

Correct operation of neuronal networks depends on the interplay between synaptic excitation and inhibition processes leading to a dynamic state termed balanced network. In the spinal cord, balanced network activity is fundamental for the expression of locomotor patterns necessary for rhythmic activation of limb extensor and flexor muscles. After spinal cord lesion, paralysis ensues often followed by spasticity. These conditions imply that, below the damaged site, the state of balanced networks has been disrupted and that restoration might be attempted by modulating the excitability of sublesional spinal neurons. Because of the widespread expression of inhibitory GABAergic neurons in the spinal cord, their role in the early and late phases of spinal cord injury deserves full attention. Thus, an early surge in extracellular GABA might be involved in the onset of spinal shock while a relative deficit of GABAergic mechanisms may be a contributor to spasticity. We discuss the role of GABA A receptors at synaptic and extrasynaptic level to modulate network excitability and to offer a pharmacological target for symptom control. In particular, it is proposed that activation of GABA A receptors with synthetic GABA agonists may downregulate motoneuron hyperexcitability (due to enhanced persistent ionic currents) and, therefore, diminish spasticity. This approach might constitute a complementary strategy to regulate network excitability after injury so that reconstruction of damaged spinal networks with new materials or cell transplants might proceed more successfully.

Indexed as

AnimalsExcitatory Postsynaptic PotentialsGABAergic NeuronsHumansInhibitory Postsynaptic PotentialsMotor NeuronsNerve NetReceptors, GABA-ASpinal CordSpinal Cord InjuriesReceptors, GABA-AGABANeuroprotectionSpasticitySpinal circuitsSpinal cord injurySpinal shock

Identifiers

PMID33826070
PMCPMC8279998
OpenAlexW3152356748

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.