dc.creator | Arumugam, Saravanan | es |
dc.creator | Garcera, Ana | es |
dc.creator | Soler, Rosa M. | es |
dc.creator | Tabares, Lucía | es |
dc.date.accessioned | 2020-04-29T16:53:18Z | |
dc.date.available | 2020-04-29T16:53:18Z | |
dc.date.issued | 2017-09-05 | |
dc.identifier.citation | Saravanan Arumugam, , Garcera, A., Soler, R.M. y Tabares Domínguez, L. (2017). Smn-Deficiency Increases the Intrinsic Excitability of Motoneurons. Frontiers in cellular neuroscience, 11 | |
dc.identifier.issn | 1662-5102 | es |
dc.identifier.uri | https://hdl.handle.net/11441/95988 | |
dc.description.abstract | During development, motoneurons experience significant changes in their size and in
the number and strength of connections that they receive, which requires adaptive
changes in their passive and active electrical properties. Even after reaching maturity,
motoneurons continue to adjust their intrinsic excitability and synaptic activity for proper
functioning of the sensorimotor circuit in accordance with physiological demands.
Likewise, if some elements of the circuit become dysfunctional, the system tries to
compensate for the alterations to maintain appropriate function. In Spinal Muscular
Atrophy (SMA), a severe motor disease, spinal motoneurons receive less excitation
from glutamatergic sensory fibers and interneurons and are electrically hyperexcitable.
Currently, the origin and relationship among these alterations are not completely
established. In this study, we investigated whether Survival of Motor Neuron (SMN), the
ubiquitous protein defective in SMA, regulates the excitability of motoneurons before
and after the establishment of the synaptic contacts. To this end, we performed patch-
clamp recordings in embryonic spinal motoneurons forming complex synaptic networks
in primary cultures, and in differentiated NSC-34 motoneuron-like cells in the absence
of synaptic contacts. Our results show that in both conditions, Smn-deficient cells
displayed lower action potential threshold, greater action potential amplitudes, and
larger density of voltage-dependent sodium currents than cells with normal Smn-levels.
These results indicate that Smn participates in the regulation of the cell-autonomous
excitability of motoneurons at an early stage of development. This finding may contribute
to a better understanding of motoneuron excitability in SMA during the development of
the disease. | es |
dc.description.sponsorship | Ministerio de Ciencia e Innovación de España / FEDER BFU2013-43763-P BFU2016-78934-P | es |
dc.description.sponsorship | Unión Europea Fondo Europeo de Desarrollo Regional (FEDER) ‘‘Una manera de hacer Europa’’ | es |
dc.description.sponsorship | Generalitat de Catalunya SGR740 | es |
dc.format | application/pdf | es |
dc.format.extent | 13 | es |
dc.language.iso | eng | es |
dc.relation.ispartof | Frontiers in cellular neuroscience, 11 | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Spinal muscular atrophy (SMA) | es |
dc.subject | Motoneurons | es |
dc.subject | Hyperexcitability | es |
dc.subject | Ion currents | es |
dc.subject | Synapses | es |
dc.title | Smn-Deficiency Increases the Intrinsic Excitability of Motoneurons | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica. | es |
dc.identifier.doi | 10.3389/fncel.2017.00269 | es |
dc.contributor.group | Universidad de Sevilla. BIO 209: Neurotransmisión y sinaptopatologías | es |
dc.journaltitle | Frontiers in cellular neuroscience | es |
dc.publication.volumen | 11 | es |