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Weight-drop model as a valuable tool to study potential neurobiological processes underlying behavioral and cognitive changes secondary to mild traumatic brain injury

2023; Elsevier BV; Volume: 385; Linguagem: Inglês

10.1016/j.jneuroim.2023.578242

1872-8421

Caroline Amaral Machado, Bruna da Silva Oliveira, Thomaz Lüscher Dias, João Luís Vieira Monteiro de Barros, Gabriel Felix, Thiago Macedo e Cordeiro, Victor Feracin, Cristian Henrique Alexandre, Larissa Katharina Sabino Abreu, Walison N. Silva, Brener Cunha Carvalho, Heliana de Barros Fernandes, Érica Leandro Marciano Vieira, Pollyana Ribeiro Castro, Rodrigo Lopes Ferreira, Lucas M. Kangussu, Glória Regina Franco, Cristina Guatimosim, Lucíola S. Barcelos, Ana Cristina Simões e Silva, Eliana Cristina de Brito Toscano, Milene Alvarenga Rachid, Antônio Lúcio Teixeira, Aline Silva de Miranda,

S100 Proteins and Annexins

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.