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dc.contributor.authorPasquini, Juana M.es
dc.contributor.authorBarrantes, Francisco Josées
dc.contributor.authorQuintá, Héctor R.es
dc.date.accessioned2019-08-01T01:37:30Z-
dc.date.available2019-08-01T01:37:30Z-
dc.date.issued2017-
dc.identifier.citationPasquini, J. M., Barrantes, F. J, Quintá, H. R. Normal development of spinal axons in early embryo stages and posterior locomotor function is independent of GAL-1 [en línea]. Journal of Comparative Neurology. 2017, 525 (13). doi:10.1002/cne.24243. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8530es
dc.identifier.issn1096-9861 (online)-
dc.identifier.issn0021-9967 (Impreso)-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/8530-
dc.description.abstractAbstract: It was recently described that Galectin-1 (Gal-1) promotes axonal growth after spinal cord injury. This effect depends on protein dimerization, since monomeric Gal-1 fails to stimulate axonal re-growth. Gal-1 is expressed in vivo at concentrations that favor the monomeric species. The aim of the present study is to investigate whether endogenous Gal-1 is required for spinal axon development and normal locomotor behavior in mice. In order to characterize axonal development, we used a novel combination of 3-DISCO technique with 1-photon microscopy and epifluorescence microscopy under high power LED illumination, followed by serial image section deconvolution and 3-D reconstruction. Cleared whole lgals-1 -/- embryos were used to analyze the 3-D cytoarchitecture of motor, commissural, and sensory axons. This approach allowed us to evaluate axonal development, including the number of fibers, fluorescence density of the fiber tracts, fiber length as well as the morphology of axonal sprouting, deep within the tissue. Gal-1 deficient embryos did not show morphological/anatomical alterations in any of the axonal populations and parameters analyzed. In addition, specific guidance receptor PlexinA4 did not change its axonal localization in the absence of Gal-1. Finally, Gal-1 deficiency did not change normal locomotor activity in post-natal animals. Taken together, our results show that development of spinal axons as well as the locomotor abilities observed in adult mice are independent of Gal-1. Supporting our previous observations, the present study further validates the use of lgals-1 -/- mice to develop spinal cord- or traumatic brain injury models for the evaluation of the regenerative action of Gal-1.es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherWileyes
dc.rightsAcceso Abierto. 1 año de embargoes
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0/es
dc.sourceJournal of Comparative Neurology. 2017, 525 (13)es
dc.subjectPROTEINASes
dc.subjectMEDULA ESPINALes
dc.subjectDESARROLLO EMBRIONARIOes
dc.subjectFUNCIONES MOTORASes
dc.titleNormal development of spinal axons in early embryo stages and posterior locomotor function is independent of GAL-1es
dc.typeArtículoes
dc.identifier.doi10.1002/cne.24243-
uca.pathFacultad de Ciencias Médicas|Instituto de Investigaciones Biomédicas (BIOMED UCA-CONICET)|Artículoses
uca.disciplinaMEDICINAes
uca.filename/home/data-uca-generic/folder_facultad/normal-development-spinal-axons/metadata.xmles
uca.issnrd1es
uca.affiliationFil: Pasquini, Juana M. Universidad de Buenos Aires. Instituto de Química y Físico Química Biológica. Departamento de Química Biológica; Argentinaes
uca.affiliationFil: Barrantes, Francisco J. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Neurobiología Molecular; Argentinaes
uca.affiliationFil: Barrantes, Francisco J. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas. Laboratorio de Neurbiología Molecular; Argentinaes
uca.affiliationFil: Quintá, Héctor R. Universidad de Buenos Aires. Instituto de Química y Físico Química Biológica. Departamento de Química Biológica; Argentinaes
uca.versionpublishedVersiones
item.grantfulltextopen-
item.fulltextWith Fulltext-
item.languageiso639-1en-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Neurobiología Molecular-
crisitem.author.deptFacultad de Ciencias Médicas-
crisitem.author.orcid0000-0002-4745-681X-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgPontificia Universidad Católica Argentina-
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