HIPPOCAMPAL NEUROGENESIS REDUCTION AFTER SPINAL CORD INJURY

JURE, IGNACIO; DE NICOLA, ALEJANDRO F.; ENCINAS JM; LABOMBARDA F

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Congreso; Encuentro de la Sociedad de Biologia; 2018

After spinal cord injury (SCI), patients exhibitcognitive deficits that could be related to hippocampal alterations. In thisregard, we have previously described microglial and astrocyte activation andneurogenesis reduction after chronic SCI in rats. In the present work we haveused the Nestin-GFP mice combined with multiple immunolabeling (BrdU, Ki67,GFAP, doublecortin, NeuN) and confocal microscopy in order to determine whichstep in the neurogenic process was altered both in the actute and chronic phaseafter spinal cord compression. Survival and mitotic capacity of radia glialcells (Nestin-GFP+/GFAP+ cells) and amplifying progenitors (Nestin-GFP +/ GFAP-cells) were assessed by labeling those cells with BrdU and/or ki67. Reactiveastrocytes were defined as star-shaped cells GFAP+/Nestin-GFP +. In the acuteperiod (7 days post injury, 7dpi) we have observed a reduction in the number ofproliferating cells (ki67 + cells), amplifying progenitors (Nestin-GFP + / GFAP-) and neuroblast (doublecortin + cells) in the dentate gyrus. The number ofcFos positive cells in the granular cell layer was decreased indicatingneuronal reduced activity that could be related to diminished neurogenesis. Wehave also found an increase in astrocyte activation in different regions of thehippocampus especially in the stratum radiatum. Fifty days after injury animalsmaintained neurogenesis reduction, astrocyte activation and the decrease incFos positive neurons indicating that SCI drove irreversible changes inneurogenesis and neuronal activity of the dentate gyrus. These hippocampalchanges could explain cognitive deficits reported in humans.