Weight-drop model as a valuable tool to study potential neurobiological processes underlying behavioral and cognitive changes secondary to mild traumatic brain injury.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Machado Caroline Amaral, Oliveira Bruna da Silva, Dias Thomaz Lüscher, Barros João Luís Vieira Monteiro de, Ferreira Gabriel Moreira Félix, Cordeiro Thiago Macedo, Feracin Victor, Alexandre Cristian Henrique, Abreu Larissa Katharina Sabino, Silva Walison Nunes da, Carvalho Brener Cunha, Fernandes Heliana de Barros, Vieira Érica Leandro Marciano, Castro Pollyana Ribeiro, Ferreira Rodrigo Novaes, Kangussu Lucas Miranda, Franco Gloria Regina, Guatimosim Cristina, Barcelos Lucíola da Silva, Simões E Silva Ana Cristina, Toscano Eliana Cristina de Brito, Rachid Milene Alvarenga, Teixeira Antônio Lúcio, Miranda Aline Silva de
Аннотация
The pathophysiology of post-traumatic brain injury (TBI) behavioral and cognitive changes is not fully understood, especially in its mild presentation. We designed a weight drop TBI model in mice to investigate the role of neuroinflammation in behavioral and cognitive sequelae following mild TBI. C57BL/6 mice displayed depressive-like behavior at 72 h after mild TBI compared with controls, as indicated by a decrease in the latency to first immobility and climbing time in the forced swim test. Additionally, anxiety-like behavior and hippocampal-associated spatial learning and memory impairment were found in the elevated plus maze and in the Barnes maze, respectively. Levels of a set of inflammatory mediators and neurotrophic factors were analyzed at 6 h, 24 h, 72 h, and 30 days after injury in ipsilateral and contralateral hemispheres of the prefrontal cortex and hippocampus. Principal components analysis revealed two principal components (PC), which represented 59.1% of data variability. PC1 (cytokines and chemokines) expression varied between both hemispheres, while PC2 (neurotrophic factors) expression varied only across the investigated brain areas. Our model reproduces mild TBI-associated clinical signs and pathological features and might be a valuable tool to broaden the knowledge regarding mild TBI pathophysiology as well as to test potential therapeutic targets.