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Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury
Few preclinical studies have assessed the long-term neuropathology and behavioral deficits after sustaining blast-induced neurotrauma (BINT). Previous studies have shown extensive astrogliosis and cell death at acute stages (<7 days) but the temporal response at a chronic stage has yet to be asce...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4633584/ https://www.ncbi.nlm.nih.gov/pubmed/26537106 http://dx.doi.org/10.1038/srep15075 |
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author | Sajja, Venkata Siva Sai Sujith Hubbard, W. Brad Hall, Christina S. Ghoddoussi, Farhad Galloway, Matthew P. VandeVord, Pamela J. |
author_facet | Sajja, Venkata Siva Sai Sujith Hubbard, W. Brad Hall, Christina S. Ghoddoussi, Farhad Galloway, Matthew P. VandeVord, Pamela J. |
author_sort | Sajja, Venkata Siva Sai Sujith |
collection | PubMed |
description | Few preclinical studies have assessed the long-term neuropathology and behavioral deficits after sustaining blast-induced neurotrauma (BINT). Previous studies have shown extensive astrogliosis and cell death at acute stages (<7 days) but the temporal response at a chronic stage has yet to be ascertained. Here, we used behavioral assays, immmunohistochemistry and neurochemistry in limbic areas such as the amygdala (Amy), Hippocampus (Hipp), nucleus accumbens (Nac), and prefrontal cortex (PFC), to determine the long-term effects of a single blast exposure. Behavioral results identified elevated avoidance behavior and decreased short-term memory at either one or three months after a single blast event. At three months after BINT, markers for neurodegeneration (FJB) and microglia activation (Iba-1) increased while index of mature neurons (NeuN) significantly decreased in all brain regions examined. Gliosis (GFAP) increased in all regions except the Nac but only PFC was positive for apoptosis (caspase-3). At three months, tau was selectively elevated in the PFC and Hipp whereas α-synuclein transiently increased in the Hipp at one month after blast exposure. The composite neurochemical measure, myo-inositol+glycine/creatine, was consistently increased in each brain region three months following blast. Overall, a single blast event resulted in enduring long-term effects on behavior and neuropathological sequelae. |
format | Online Article Text |
id | pubmed-4633584 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-46335842015-11-05 Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury Sajja, Venkata Siva Sai Sujith Hubbard, W. Brad Hall, Christina S. Ghoddoussi, Farhad Galloway, Matthew P. VandeVord, Pamela J. Sci Rep Article Few preclinical studies have assessed the long-term neuropathology and behavioral deficits after sustaining blast-induced neurotrauma (BINT). Previous studies have shown extensive astrogliosis and cell death at acute stages (<7 days) but the temporal response at a chronic stage has yet to be ascertained. Here, we used behavioral assays, immmunohistochemistry and neurochemistry in limbic areas such as the amygdala (Amy), Hippocampus (Hipp), nucleus accumbens (Nac), and prefrontal cortex (PFC), to determine the long-term effects of a single blast exposure. Behavioral results identified elevated avoidance behavior and decreased short-term memory at either one or three months after a single blast event. At three months after BINT, markers for neurodegeneration (FJB) and microglia activation (Iba-1) increased while index of mature neurons (NeuN) significantly decreased in all brain regions examined. Gliosis (GFAP) increased in all regions except the Nac but only PFC was positive for apoptosis (caspase-3). At three months, tau was selectively elevated in the PFC and Hipp whereas α-synuclein transiently increased in the Hipp at one month after blast exposure. The composite neurochemical measure, myo-inositol+glycine/creatine, was consistently increased in each brain region three months following blast. Overall, a single blast event resulted in enduring long-term effects on behavior and neuropathological sequelae. Nature Publishing Group 2015-11-05 /pmc/articles/PMC4633584/ /pubmed/26537106 http://dx.doi.org/10.1038/srep15075 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Sajja, Venkata Siva Sai Sujith Hubbard, W. Brad Hall, Christina S. Ghoddoussi, Farhad Galloway, Matthew P. VandeVord, Pamela J. Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury |
title | Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury |
title_full | Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury |
title_fullStr | Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury |
title_full_unstemmed | Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury |
title_short | Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury |
title_sort | enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4633584/ https://www.ncbi.nlm.nih.gov/pubmed/26537106 http://dx.doi.org/10.1038/srep15075 |
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