Premium
Juvenile mild traumatic brain injury elicits distinct spatiotemporal astrocyte responses
Author(s) -
Clément Tifenn,
Lee Jeong B.,
Ichkova Aleksandra,
RodriguezGrande Beatriz,
Fournier MarieLine,
Aussudre Justine,
Ogier Michael,
Haddad Elizabeth,
Canini Frederic,
Koehl Muriel,
Abrous Djoher Nora,
Obenaus Andre,
Badaut Jerome
Publication year - 2020
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.23736
Subject(s) - astrogliosis , glial fibrillary acidic protein , neuroscience , traumatic brain injury , astrocyte , dentate gyrus , hippocampal formation , nestin , context (archaeology) , medicine , pathology , prefrontal cortex , psychology , amygdala , biology , central nervous system , cognition , neural stem cell , immunohistochemistry , microbiology and biotechnology , psychiatry , paleontology , stem cell
Mild‐traumatic brain injury (mTBI) represents ~80% of all emergency room visits and increases the probability of developing long‐term cognitive disorders in children. To date, molecular and cellular mechanisms underlying post‐mTBI cognitive dysfunction are unknown. Astrogliosis has been shown to significantly alter astrocytes' properties following brain injury, potentially leading to significant brain dysfunction. However, such alterations have never been investigated in the context of juvenile mTBI (jmTBI). A closed‐head injury model was used to study jmTBI on postnatal‐day 17 mice. Astrogliosis was evaluated using glial fibrillary acidic protein (GFAP), vimentin, and nestin immunolabeling in somatosensory cortex (SSC), dentate gyrus (DG), amygdala (AMY), and infralimbic area (ILA) of prefrontal cortex in both hemispheres from 1 to 30 days postinjury (dpi). In vivo T2‐weighted‐imaging (T2WI) and diffusion tensor imaging (DTI) were performed at 7 and 30 dpi to examine tissue level structural alterations. Increased GFAP‐labeling was observed up to 30 dpi in the ipsilateral SSC, the initial site of the impact. However, vimentin and nestin expression was not perturbed by jmTBI. The morphology of GFAP positive cells was significantly altered in the SSC, DG, AMY, and ILA up to 7 dpi that some correlated with magnetic resonance imaging changes. T2WI and DTI values were significantly altered at 30 dpi within these brain regions most prominently in regions distant from the impact site. Our data show that jmTBI triggers changes in astrocytic phenotype with a distinct spatiotemporal pattern. We speculate that the presence and time course of astrogliosis may contribute to pathophysiological processes and long‐term structural alterations following jmTBI.