NEUROINFLAMATORY-RELATED PROCESES AND COGNITIVE DEFICITS INDUCED BY AN ANIMAL MODEL OF TRAUMATIC BRAIN INJURY: CHARACTERIZATION OF TEMPORAL COURSE

MARISA GHERSI,; AGUSTIN MONTIVERO; FLORENCIA CONSTANTIN; ELIZABETH HEER; MARIELA F. PEREZ

Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017

SAIC

Brain damage caused by acute trauma (TBI) is associated withhigh morbidity and mortality. In Argentina is considered the leadingcause of disability in children and young adults.TBI is a complex disordercaused by primary and secondary injury mechanisms. Primarymechanisms are the result of mechanical damage. Secondary injuryprogresses (SI) begin after minutes, or even months after the initialtrauma as a result of neurochemical, metabolic and cellular changes.These secondary events are believed to underlie the developmentof many neurological deficits.The aim of the present investigation isto elucidate the temporal course of SI related to neuroinflamationand cognitive deficits induced in an animal model of TBI, to find asuitable window time for pharmacological intervention. For this purposewe used a closed head impact controlled by weight dropas ananimal model of TBI. Animals were evaluated clinically immediatelypost TBI (hart and respiratory rate and apnea), and 60 min, 24 hand 7 days after TBI, were sacrificed to measure glia inflammationlabeling GFAP (astrocytes) and CD11b (microglia) by immunohistochemistry(IHC). Also, Barnes Maze was performed 24 h post TBI toevaluate spatial memory. Our results showed increased glial activationprofiles in hippocampus at 60 min and 24 h, returning to SHAMvalues at 7 days post TBI. No differences between SHAM and TBIgroups were observed in behavioral performance. IHC and behavioraldata were analyzed by one way ANOVA or t-test respectively.In conclusion, our data suggest that the neuroinflamation observedearly after TBI did not affect a hippocampal-dependent memory acquisitionand retrieval, at the timeevaluated. As described by otherauthors, these deficits could be observed long term after TBI as aconsequence of early neuroinflamation. Further studies need to beperformed to evaluate this possibility and to complete the neuroinflamatoryprofile.