INVESTIGADORES
LABOMBARDA Maria Florencia
congresos y reuniones científicas
Título:
Brain responses after a distant chronic spinal cord injury.
Autor/es:
JURE, I; DE NICOLA A; LABOMBARDA F
Lugar:
Mar del plata
Reunión:
Congreso; XXX Congreso anual de la Sociedad Argentina de Investigación en Neurociencias; 2015
Resumen:
Central nervous insults, such asspinal cord injury (SCI) or traumatic brain injury, are among the leadingcauses of mortality and morbidity worldwide. They produce profound neurologicaldysfunction, due to the progressive destruction of local and distal neuronalnetworks. The impact of SCI has long focused on motor deficits or suchsecondary complications as neuropathic pain, compromised bladder/bowelfunction, loss of sexual function, or emotional distress. Cognitive deficitshave been reported after SCI and its prevalence has likely been underestimated.Here we examined effects of chronic thoracic SCI on the activation ofmicroglial cells in the hippocampus and the effects on SGZ neurogenesis. Weused a clip compression model of SCI and performed two kinds of lesion, onemoderate and one severe in rats. We studied by immunohistochemistry the numberof ramified and hypertrophic/bushy microglial cells (Ox-42 + cells) and thenumber of doublecortin positive cells (an index of neurogenesis)  in the hippocampus. Our results shown that 60days after injury (60 dpi) there was an increased in the number of activatedhypertrophic/busy microglia at hippocampus hilus in the moderate and severe SCImodels. In addtion, the density of activated hypertrophic/busy microglia was upregulated only in the severe model of SCI at the stratum radiatum of the CA1and CA3 region of the hippocampus. The number of ramified microglia cells didnot change in any studied group. Next, we explored neurogenesis at the SGZ ofthe hippocampus, and we observed that doublecortin + cells were down regulated60 dpi in the moderate and severe model of SCI compared to intact rats. Inconclusion, our results suggested that chronic brain neuroinflammationcould occur after chronic SCI, likely related to sustained microglialactivation. Microglial activation could reduce neurogenesis at the hippocampusand be related to cognitive deficits reported inpatients.