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dc.contributor.author
Mazzone, Graciela Luján
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dc.contributor.author
Mohammadshirazi, Atiyeh
dc.contributor.author
Aquino, Jorge Benjamin
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dc.contributor.author
Nistri, Andrea
dc.contributor.author
Taccola, Giuliano
dc.date.available
2023-01-19T18:19:04Z
dc.date.issued
2021-04
dc.identifier.citation
Mazzone, Graciela Luján; Mohammadshirazi, Atiyeh; Aquino, Jorge Benjamin; Nistri, Andrea; Taccola, Giuliano; GABAergic Mechanisms Can Redress the Tilted Balance between Excitation and Inhibition in Damaged Spinal Networks; Springer; Molecular Neurobiology; 58; 8; 4-2021; 3769-3786
dc.identifier.issn
0893-7648
dc.identifier.uri
http://hdl.handle.net/11336/185064
dc.description.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.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Springer
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by/2.5/ar/
dc.subject
GABA
dc.subject
NEUROPROTECTION
dc.subject
SPASTICITY
dc.subject
SPINAL CIRCUITS
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SPINAL CORD INJURY
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SPINAL SHOCK
dc.subject.classification
Neurociencias
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
GABAergic Mechanisms Can Redress the Tilted Balance between Excitation and Inhibition in Damaged Spinal Networks
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2022-09-21T14:15:10Z
dc.journal.volume
58
dc.journal.number
8
dc.journal.pagination
3769-3786
dc.journal.pais
Alemania
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dc.journal.ciudad
Berlín
dc.description.fil
Fil: Mazzone, Graciela Luján. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina
dc.description.fil
Fil: Mohammadshirazi, Atiyeh. Scuola Internazionale Superiore Di Studi Avanzati (sissa);
dc.description.fil
Fil: Aquino, Jorge Benjamin. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina
dc.description.fil
Fil: Nistri, Andrea. Scuola Internazionale Superiore Di Studi Avanzati (sissa);
dc.description.fil
Fil: Taccola, Giuliano. Scuola Internazionale Superiore Di Studi Avanzati (sissa);
dc.journal.title
Molecular Neurobiology
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007/s12035-021-02370-5
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1007/s12035-021-02370-5
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