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Subventricular zone neural precursor cell responses after traumatic brain injury and binge alcohol in male rats.
Ton, Son T; Tsai, Shih-Yen; Vaagenes, Ian C; Glavin, Kelly; Wu, Joanna; Hsu, Jonathan; Flink, Hannah M; Nockels, Daniel; O'Brien, Timothy E; Kartje, Gwendolyn L.
Afiliação
  • Ton ST; Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.
  • Tsai SY; Department of Molecular Pharmacology and Therapeutics, Loyola University Chicago Health Sciences Division, Maywood, Illinois.
  • Vaagenes IC; Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.
  • Glavin K; Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.
  • Wu J; Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.
  • Hsu J; Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.
  • Flink HM; Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.
  • Nockels D; Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.
  • O'Brien TE; Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois.
  • Kartje GL; Department of Mathematics and Statistics, Institute of Environmental Sustainability, Loyola University Chicago, Chicago, Illinois.
J Neurosci Res ; 97(5): 554-567, 2019 05.
Article em En | MEDLINE | ID: mdl-30614539
ABSTRACT
Traumatic brain injury (TBI) is a major cause of disability worldwide. Additionally, many TBI patients are intoxicated with alcohol at the time of injury, but the impact of acute intoxication on recovery from brain injury is not well understood. We have previously found that binge alcohol prior to TBI impairs spontaneous functional sensorimotor recovery. However, whether alcohol administration in this setting affects reactive neurogenesis after TBI is not known. This study, therefore, sought to determine the short- and long-term effects of pre-TBI binge alcohol on neural precursor cell responses in the subventricular zone (SVZ) following brain injury in male rats. We found that TBI alone significantly increased proliferation in the SVZ as early as 24 hr after injury. Surprisingly, binge alcohol alone also significantly increased proliferation in the SVZ after 24 hr. However, a combined binge alcohol and TBI regimen resulted in decreased TBI-induced proliferation in the SVZ at 24 hr and 1 week post-TBI. Furthermore, at 6 weeks after TBI, binge alcohol administered at the time of TBI significantly decreased the TBI-induced neuroblast response in the SVZ and the rostral migratory stream (RMS). The results from this study suggest that pre-TBI binge alcohol negatively impacts reparative processes in the brain by decreasing short-term neural precursor cell proliferative responses as well as long-term neuroblasts in the SVZ and RMS.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Ventrículos Cerebrais / Células-Tronco Neurais / Consumo Excessivo de Bebidas Alcoólicas / Lesões Encefálicas Traumáticas Limite: Animals Idioma: En Revista: J Neurosci Res Ano de publicação: 2019 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Ventrículos Cerebrais / Células-Tronco Neurais / Consumo Excessivo de Bebidas Alcoólicas / Lesões Encefálicas Traumáticas Limite: Animals Idioma: En Revista: J Neurosci Res Ano de publicação: 2019 Tipo de documento: Article
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