SPINAL CORD INJURY IMPAIRS NEUROGENESIS AND INDUCES GLIAL REACTIVITY IN THE HIPPOCAMPUS

JURE IGNACIO; LUCIANA PIETRANERA; ALEJANDRO F. DE NICOLA; FLORENCIA LABOMBARDA

NEUROCHEMICAL RESEARCH

SPRINGER/PLENUM PUBLISHERS

Lugar: New York; Año: 2017 vol. 42 p. 2178 - 2190

0364-3190

Theincorporation of newborn neurons with increased synaptic remodeling andactivity-dependent plasticity in the dentate gyrus enhanceshippocampal-dependent learning performances. Astrocytes and microglial cellsare components of the neurogenic niche and regulate neurogenesis under normal andneurophatological conditions leading to functional consequences for learningand memory. Although cognitive impairments were reported in patients afterspinal cord injury (SCI), only few studies have considered remote changes inbrain structures which are not related with sensory and motor cortex. Thus, weexamined neurogenesis and glial reactivity by stereological assessment in dentategyrus sub-regions after three different intensities of thoracic spinal cordcompression in rats. Sixty days after injury we observed a decrease in the Basso-Bresnahan?Beattie locomotor scale scores,rotarod performance and volume of spare tissue that correlated with theseverity of the compression.  Regardingthe hippocampus, we observed that neurogenesis andneuronal hilar neurons were reduced after severe SCI, while only neurogenesisdecreased in the moderately injured group. In addition, severe SCI inducedreactive microglia and astrogliosis in all the dentategyrus sub-regions. Furthermore, the density of reactive microglia increased inthe hilus whereas astrogliosis developed in the molecular layer after moderateSCI. No changes were observed in the mildly injured rats. These results suggestthat glial response and neurogenesis are associated with injury intensity. Interestingly,hippocampal neurogenesis is more sensitive to SCI than astrocytes or microglia,as moderate injury impairs the generation of new neurons without changing glialresponse in subgranular zone.