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dc.contributor.authorMercadante, Marcos Tomanik [UNIFESP]
dc.contributor.authorCysneiros, Roberta Monterazzo
dc.contributor.authorSchwartzman, Jose Salomao
dc.contributor.authorArida, Ricardo Mario [UNIFESP]
dc.contributor.authorCavalheiro, Esper Abrao [UNIFESP]
dc.contributor.authorScorza, Fulvio Alexandre [UNIFESP]
dc.date.accessioned2016-01-24T13:49:23Z
dc.date.available2016-01-24T13:49:23Z
dc.date.issued2008-01-01
dc.identifierhttp://dx.doi.org/10.1016/j.mehy.2007.05.018
dc.identifier.citationMedical Hypotheses. Edinburgh: Churchill Livingstone, v. 70, n. 2, p. 352-357, 2008.
dc.identifier.issn0306-9877
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/30287
dc.description.abstractNeurogenesis studies had an increased development after BrdU (5-bromo-3'-deoxyuridine), a marker of cell proliferation. Today, several studies have showed the relevance of neurogenesis in the hippocampal formation. Notwithstanding, other brains areas have been described presenting neurogenesis, including the amygdata. This key structure is a complex cerebral region which has been associated with social behaviors and the emotional significance of the daily experiences. Several studies have associated the amygdala to the autism, a severe neurodevetopmentat disorder. in this paper, we discuss the hypothesis of neurogenesis in the amygdata as a contributing cause of autism. the social skills require competent new neuronal connections, including efficient plasticity synaptic rearranging. Interestingly, emotional context cannot be imprinting in mature neurons in the presence of GABA, a neurotransmitter release during new environments experiences. However, it is known that new neurons are not welt responsive to GABA stimulation, allowing the tong-term potentiation necessary for the learning process. Based on these evidence it is tantalizing to hypothesize that the sociability impairment seen in some individuals with autism may partly be assigned to impaired regulation of the GABAergic system and to the impact of this impairment on the adequate functioning of the annygdala and on its capacity to store new experiences and to modulate the plasticity of the corticostriatal connections. (c) 2007 Elsevier B.V. All rights reserved.en
dc.format.extent352-357
dc.language.isoeng
dc.publisherChurchill Livingstone
dc.relation.ispartofMedical Hypotheses
dc.rightsAcesso restrito
dc.titleNeurogenesis in the amygdala: A new etiologic hypothesis of autism?en
dc.typeArtigo
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionCent Univ Sao Camilo
dc.contributor.institutionUniv Presbyterian Mackenzie
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Dept Psychiat, UNIFESP EPM, BR-04023900 São Paulo, Brazil
dc.description.affiliationCent Univ Sao Camilo, Dept Pharmacol, São Paulo, Brazil
dc.description.affiliationUniv Presbyterian Mackenzie, Pervas Dev Disorders Program, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, UNIFESP EPM, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, UNIFESP EPM, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Dept Psychiat, UNIFESP EPM, BR-04023900 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, UNIFESP EPM, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, UNIFESP EPM, São Paulo, Brazil
dc.identifier.doi10.1016/j.mehy.2007.05.018
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000252901500032


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