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Neurobiological substrates underlying corpus callosum hypoconnectivity and brain metabolic patterns in the valproic acid rat model of autism spectrum disorder

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dc.contributor.author Uccelli, Nonthué Alejandra
dc.contributor.author Codagnone, Martín Gabriel
dc.contributor.author Traetta, Marianela Evelyn
dc.contributor.author Levanovich, Nadia
dc.contributor.author Rosato-Siri, María Victoria
dc.contributor.author Urrutia, Leandro
dc.contributor.author Falasco, Germán
dc.contributor.author Vázquez, Silvia
dc.contributor.author Pasquini, Juana María
dc.contributor.author Reinés, Analía Gabriela
dc.date.accessioned 2021-06-16T14:26:45Z
dc.date.available 2021-06-16T14:26:45Z
dc.date.issued 2021-06-03
dc.identifier.citation Uccelli NA, Codagnone MG, Traetta ME, Levanovich N, Rosato Siri MV, Urrutia L, Falasco G, Vázquez S, Pasquini JM, Reinés AG. Neurobiological substrates underlying corpus callosum hypoconnectivity and brain metabolic patterns in the valproic acid rat model of autism spectrum disorder. J Neurochem. 2021 Jun 3. doi: 10.1111/jnc.15444 es_ES
dc.identifier.uri https://doi.org/10.1111/jnc.15444
dc.identifier.uri https://repositorio.fleni.org.ar/xmlui/handle/123456789/496
dc.description.abstract Atypical connectivity between brain regions and altered structure of the corpus callosum (CC) in imaging studies support the long-distance hypoconnectivity hypothesis proposed for autism spectrum disorder (ASD). The aim of this study was to unveil the CC ultrastructural and cellular changes employing the valproic acid (VPA) rat model of ASD. Male Wistar rats were exposed to VPA (450 mg/kg i.p.) or saline (control) during gestation (embryonic day 10.5), and maturation, exploration and social behavior were subsequently tested. Myelin content, ultrastructure and oligodendroglial lineage were studied in the CC at postnatal day 15 (infant) and 36 (juvenile). As a functional outcome, brain metabolic activity was determined by positron emission tomography. Concomitantly with behavioral deficits in juvenile VPA rats, the CC showed reduced myelin basic protein, conserved total number of axons, reduced percentage of myelinated axons and aberrant and less compact arrangements of myelin sheath ultrastructure. Mature oligodendrocytes decreased and oligodendrocyte precursors increased in the absence of astrogliosis or microgliosis. In medial prefrontal and somatosensory cortices of juvenile VPA rats, myelin ultrastructure and oligodendroglial lineage were preserved. VPA animals exhibited global brain hypometabolism and local hypermetabolism in brain regions relevant for ASD. In turn, the CC of infant VPA rats showed reduced myelin content but preserved oligodendroglial lineage. Our findings indicate that CC hypomyelination is established during infancy and prior to oligodendroglial pattern alterations, which suggests that axon-oligodendroglia communication could be compromised in VPA animals. Thus, CC hypomyelination may underlie white matter alterations and contribute to atypical patterns of connectivity and metabolism found in ASD. es_ES
dc.language.iso eng es_ES
dc.publisher Wiley es_ES
dc.rights info:eu-repo/semantics/openAccess
dc.rights.uri https://creativecommons.org/licenses/by/2.5/ar/
dc.subject Autism Spectrum Disorder es_ES
dc.subject Trastorno del Espectro Autista es_ES
dc.subject Corpus Callosum es_ES
dc.subject Cuerpo Calloso es_ES
dc.subject Valproic Acid es_ES
dc.subject Ácido Valproico es_ES
dc.title Neurobiological substrates underlying corpus callosum hypoconnectivity and brain metabolic patterns in the valproic acid rat model of autism spectrum disorder es_ES
dc.type info:eu-repo/semantics/article es_ES
dc.type info:eu-repo/semantics/publishedVersion
dc.description.fil Fil: Uccelli, Nonthué Alejandra. Universidad de Buenos Aires. Instituto de Biología Celular y Neurociencia "Prof. E. De Robertis". Argentina.
dc.description.fil Fil: Codagnone, Martín Gabriel. Universidad de Buenos Aires. Instituto de Biología Celular y Neurociencia "Prof. E. De Robertis"; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina.
dc.description.fil Fil: Traetta, Marianela Evelyn. Universidad de Buenos Aires. Instituto de Biología Celular y Neurociencia "Prof. E. De Robertis"; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina.
dc.description.fil Fil: Levanovich, Nadia. Fleni. Departamento de Diagnóstico por Imágenes. Centro de Imágenes Moleculares; Argentina.
dc.description.fil Fil: Rosato-Siri, María Victoria. Universidad de Buenos Aires. Instituto de Química y Fisicoquímica Biológica; Argentina.
dc.description.fil Fil: Urrutia, Leandro. Fleni. Departamento de Diagnóstico por Imágenes. Centro de Imágenes Moleculares; Argentina.
dc.description.fil Fil: Falasco, Germán. Fleni. Departamento de Diagnóstico por Imágenes. Centro de Imágenes Moleculares; Argentina.
dc.description.fil Fil: Vázquez, Silvia. Fleni. Departamento de Diagnóstico por Imágenes. Centro de Imágenes Moleculares; Argentina.
dc.description.fil Fil: Pasquini, Juana María. Universidad de Buenos Aires. Instituto de Química y Fisicoquímica Biológica; Argentina.
dc.description.fil Fil: Reinés, Analía Gabriela. Universidad de Buenos Aires. Instituto de Biología Celular y Neurociencia "Prof. E. De Robertis"; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina.
dc.relation.ispartofCOUNTRY Estados Unidos
dc.relation.ispartofCITY Nueva York
dc.relation.ispartofTITLE Journal of neurochemistry
dc.relation.ispartofISSN 1471-4159
dc.type.snrd info:ar-repo/semantics/artículo es_ES


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