Estudo de alterações comportamentais e cognitivas associadas a processos inflamatórios em modelo experimental de traumatismo cranioencefálico leve

Abstract

Traumatic brain injury (TBI) is a cerebral lesion caused by an external mechanical force against the skull. TBI is the leading cause of death and disability, especially among children and young adults. Many studies have associated TBI with the development of neuropsychiatric and cognitive deficits after the traumatic event, including depression, anxiety and impairment in learning and memory. Moreover, several studies have shown that inflammatory processes may be related to the evolution of secondary lesions, as well as to the development of neuropsychiatric disorders after traumatic event. In this context, the main objective of this study was to investigate the role of inflammatory processes in the development of transient and permanent behavioral changes in the experimental model of mild TBI. For this, the model of experimental TBI by weight loss was standardized using male mice of the C57BL / 6 lineage that were evaluated in behavioral and cognitive tests standardized after the injury. With the standardized lesion protocol, no change in body weight was found and the mice presented low mortality and recovery of neurological damage after the first 6 hours after TBI. Histopathological analyzes of the brain were performed by microscopy techniques and the evaluation of inflammatory mediators was performed by CBA (Citometric Bead Array). Histopathological analyzes revealed neutrophil infiltration and hemorrhage in the cortex 6 hours after TBI. The animals presented anxiety-like behavior 12 hour and were maintained up to 30 days after the TBI and presented depressive-like behavior 72 hours after the injury. Associated with these behavioral changes, was found variations in cytokines interleukin (IL) 10 and tumor necrosis factor (TNF) levels in the prefrontal cortex and the hippocampus of the mice at different times after injury. These results show that the standardized TBI model was able to generate a lesion compatible with a mild TBI, in addition, they suggest that neuroinflammatory processes may have involvement in the behavioral changes in mice submitted to the experimental model of mild TBI.