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 (

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Veröffentlicht in:Scientific reports 2015-11, Vol.5 (1), p.15075-15075, Article 15075
Hauptverfasser: Sajja, Venkata Siva Sai Sujith, Hubbard, W. Brad, Hall, Christina S., Ghoddoussi, Farhad, Galloway, Matthew P., VandeVord, Pamela J.
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container_title Scientific reports
container_volume 5
creator Sajja, Venkata Siva Sai Sujith
Hubbard, W. Brad
Hall, Christina S.
Ghoddoussi, Farhad
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VandeVord, Pamela J.
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 (
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Brad ; Hall, Christina S. ; Ghoddoussi, Farhad ; Galloway, Matthew P. ; VandeVord, Pamela J.</creator><creatorcontrib>Sajja, Venkata Siva Sai Sujith ; Hubbard, W. Brad ; Hall, Christina S. ; Ghoddoussi, Farhad ; Galloway, Matthew P. ; VandeVord, Pamela J.</creatorcontrib><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 (&lt;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.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep15075</identifier><identifier>PMID: 26537106</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 14/63 ; 140/131 ; 59 ; 631/378/1595/1554 ; 631/378/1934 ; 631/378/371 ; alpha-Synuclein - metabolism ; Amygdala ; Amygdala - metabolism ; Amygdala - pathology ; Animals ; Apoptosis ; Apoptosis - physiology ; Avoidance behavior ; Behavior ; Brain Injuries - metabolism ; Brain Injuries - pathology ; Caspase ; Caspase 3 - metabolism ; Caspase-3 ; Cell death ; Complications ; Creatine ; Disease Models, Animal ; Glial fibrillary acidic protein ; Gliosis ; Gliosis - metabolism ; Gliosis - pathology ; Glycine ; Hippocampus - metabolism ; Hippocampus - pathology ; Humanities and Social Sciences ; Inositol ; Long-term effects ; Male ; Memory, Short-Term - physiology ; Microglia ; multidisciplinary ; Neurodegeneration ; Neurodegenerative Diseases - metabolism ; Neurodegenerative Diseases - pathology ; Neurons - metabolism ; Neurons - pathology ; Nucleus accumbens ; Nucleus Accumbens - metabolism ; Nucleus Accumbens - pathology ; Prefrontal cortex ; Prefrontal Cortex - metabolism ; Prefrontal Cortex - pathology ; Rats ; Rats, Sprague-Dawley ; Science ; Short term memory ; Synuclein ; Tau protein ; Temporal lobe ; Traumatic brain injury</subject><ispartof>Scientific reports, 2015-11, Vol.5 (1), p.15075-15075, Article 15075</ispartof><rights>The Author(s) 2015</rights><rights>Copyright Nature Publishing Group Nov 2015</rights><rights>Copyright © 2015, Macmillan Publishers Limited 2015 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-ccfdf8945a23b317637cddff5817a3597b81fd2c256a2d4438d7dc9eefe7a6443</citedby><cites>FETCH-LOGICAL-c504t-ccfdf8945a23b317637cddff5817a3597b81fd2c256a2d4438d7dc9eefe7a6443</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4633584/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4633584/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26537106$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sajja, Venkata Siva Sai Sujith</creatorcontrib><creatorcontrib>Hubbard, W. Brad</creatorcontrib><creatorcontrib>Hall, Christina S.</creatorcontrib><creatorcontrib>Ghoddoussi, Farhad</creatorcontrib><creatorcontrib>Galloway, Matthew P.</creatorcontrib><creatorcontrib>VandeVord, Pamela J.</creatorcontrib><title>Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><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 (&lt;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. 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Brad</au><au>Hall, Christina S.</au><au>Ghoddoussi, Farhad</au><au>Galloway, Matthew P.</au><au>VandeVord, Pamela J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2015-11-05</date><risdate>2015</risdate><volume>5</volume><issue>1</issue><spage>15075</spage><epage>15075</epage><pages>15075-15075</pages><artnum>15075</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>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 (&lt;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.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26537106</pmid><doi>10.1038/srep15075</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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subjects 13/51
14/63
140/131
59
631/378/1595/1554
631/378/1934
631/378/371
alpha-Synuclein - metabolism
Amygdala
Amygdala - metabolism
Amygdala - pathology
Animals
Apoptosis
Apoptosis - physiology
Avoidance behavior
Behavior
Brain Injuries - metabolism
Brain Injuries - pathology
Caspase
Caspase 3 - metabolism
Caspase-3
Cell death
Complications
Creatine
Disease Models, Animal
Glial fibrillary acidic protein
Gliosis
Gliosis - metabolism
Gliosis - pathology
Glycine
Hippocampus - metabolism
Hippocampus - pathology
Humanities and Social Sciences
Inositol
Long-term effects
Male
Memory, Short-Term - physiology
Microglia
multidisciplinary
Neurodegeneration
Neurodegenerative Diseases - metabolism
Neurodegenerative Diseases - pathology
Neurons - metabolism
Neurons - pathology
Nucleus accumbens
Nucleus Accumbens - metabolism
Nucleus Accumbens - pathology
Prefrontal cortex
Prefrontal Cortex - metabolism
Prefrontal Cortex - pathology
Rats
Rats, Sprague-Dawley
Science
Short term memory
Synuclein
Tau protein
Temporal lobe
Traumatic brain injury
title Enduring deficits in memory and neuronal pathology after blast-induced traumatic brain injury
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