Spinal Cord Injury Leads to Hippocampal Glial Alterations and Neural Stem Cell Inactivation
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ORIGINAL RESEARCH
Spinal Cord Injury Leads to Hippocampal Glial Alterations and Neural Stem Cell Inactivation Ignacio Jure1 · Alejandro F. De Nicola1,3 · Juan Manuel Encinas2 · Florencia Labombarda1,3 Received: 19 February 2020 / Accepted: 6 June 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract The hippocampus encodes spatial and contextual information involved in memory and learning. The incorporation of new neurons into hippocampal networks increases neuroplasticity and enhances hippocampal-dependent learning performances. Only few studies have described hippocampal abnormalities after spinal cord injury (SCI) although cognitive deficits related to hippocampal function have been reported in rodents and even humans. The aim of this study was to characterize in further detail hippocampal changes in the acute and chronic SCI. Our data suggested that neurogenesis reduction in the acute phase after SCI could be due to enhanced death of amplifying neural progenitors (ANPs). In addition, astrocytes became reactive and microglial cells increased their number in almost all hippocampal regions studied. Glial changes resulted in a non-inflammatory response as the mRNAs of the major pro-inflammatory cytokines (IL-1β, TNFα, IL-18) remained unaltered, but CD200R mRNA levels were downregulated. Long-term after SCI, astrocytes remained reactive but on the other hand, microglial cell density decreased. Also, glial cells induced a neuroinflammatory environment with the upregulation of IL-1β, TNFα and IL-18 mRNA expression and the decrease of CD200R mRNA. Neurogenesis reduction may be ascribed at later time points to inactivation of neural stem cells (NSCs) and inhibition of ANP proliferation. The number of granular cells and CA1 pyramidal neurons decreased only in the chronic phase. The release of pro-inflammatory cytokines at the chronic phase might involve neurogenesis reduction and neurodegeneration of hippocampal neurons. Therefore, SCI led to hippocampal changes that could be implicated in cognitive deficits observed in rodents and humans. Keywords Adult neurogenesis · Spinal cord injury · Glial alterations · Neuroinflammation
Introduction
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10571-020-00900-8) contains supplementary material, which is available to authorized users. * Florencia Labombarda [email protected] 1
Laboratory of Neuroendocrine Biochemistry, IBYME‑CONICET., Instituto de Biologia Y Medicina Experimental, Vuelta de Obligado 2490, 1428 Buenos Aires, Argentina
2
Laboratory of Neural Stem Cells and Neurogenesis, Achucarro Basque Center for Neuroscience. Sede Bldg. Campus, UPV/EHU, Barrio Sarriena S/N, 48940 Leioa, Spain
3
Department of Human Biochemistry, School of Medicine, Buenos Aires University, Paraguay 2155, C1121A6B Buenos Aires, Argentina
Traumatic spinal cord injury (SCI) is a physically disabling and psychologically devastating condition that affects mostly young healthy people in their
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