Alteraciones Hipocampales luego de una lesión espinal: un daño sin fronteras.

LABOMBARDA F

Junin

Congreso; Congreso Multidiciplinario de la UNNOBA; 2018

After spinal cord injury (SCI), patientsexhibit cognitive deficits that could be related to hippocampal alterations. Inthis regard, we have previously described microglial and astrocyte activationand neurogenesis reduction after chronic SCI in rats. In the present work wehave used the Nestin-GFP mice combined with multiple immunolabeling (BrdU,Ki67, GFAP, doublecortin, NeuN) and confocal microscopy in order to determinewhich step in the neurogenic process was altered both in the acute and chronicphases after spinal cord compression. Survival and mitotic capacity of radiaglial cells (Nestin-GFP+/GFAP+ cells) and amplifying progenitors (Nestin-GFP +/GFAP- cells) were assessed by labeling those cells with BrdU and/or ki67.Reactive astrocytes were defined as star-shaped cells GFAP+/Nestin-GFP +. Inthe acute period (7 days post injury, 7dpi) we have observed a reduction in thenumber of proliferating cells (ki67 + cells), amplifying progenitors (Nestin-GFP+ / GFAP -) and neuroblast (doublecortin + cells) in the dentate gyrus. Thenumber of cFos positive cells in the granular cell layer was decreasedindicating neuronal reduced activity that could be related to diminishedneurogenesis. We have also found an increase in astrocyte activation indifferent regions of the hippocampus especially in the stratum radiatum. Fiftydays after injury animals maintained neurogenesis reduction, astrocyteactivation and a decrease in cFos positive neurons indicating that SCI droveirreversible changes in neurogenesis and neuronal activity of the dentategyrus. These hippocampal changes could explain cognitive deficits reported inhumans.