CONICET | Buscador de Institutos y Recursos Humanos

Brain damage caused by acute trauma (TBI) is associated with high morbidity and mortality. In Argentina is considered the leading cause of disability in children and young adults.TBI is a complex disorder caused by primary and secondary injury mechanisms. Primary mechanisms are the result of mechanical damage. Secondary injury progresses (SI) begin after minutes, or even months after the initial trauma as a result of neurochemical, metabolic and cellular changes. These secondary events are believed to underlie the development of many neurological deficits.The aim of the present investigation is to elucidate the temporal course of SI related to neuroinflamation and cognitive deficits induced in an animal model of TBI, to find a suitable window time for pharmacological intervention. For this purpose we used a closed head impact controlled by weight dropas an animal model of TBI. Animals were evaluated clinically immediately post TBI (hart and respiratory rate and apnea), and 60 min, 24 h and 7 days after TBI, were sacrificed to measure glia inflammation labeling GFAP (astrocytes) and CD11b (microglia) by immunohistochemistry (IHC). Also, Barnes Maze was performed 24 h post TBI to evaluate spatial memory. Our results showed increased glial activation profiles in hippocampus and motor cortex at 60 min and 24 h, returning to SHAM values at 7 days post TBI. No differences between SHAM and TBI groups were observed in behavioral performance. IHC and behavioral data were analyzed by one way ANOVA or t-test respectively. In conclusion, our data suggest that the neuroinflamation observed early after TBI did not affect a hippocampal-dependent memory acquisition and retrieval, at the timeevaluated. As described by other authors, these deficits could be observed long term after TBI as a consequence of early neuroinflamation. Further studies need to be performed to evaluate this possibility and to complete the neuroinflamatory profile.