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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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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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 (<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><subject>13/51</subject><subject>14/63</subject><subject>140/131</subject><subject>59</subject><subject>631/378/1595/1554</subject><subject>631/378/1934</subject><subject>631/378/371</subject><subject>alpha-Synuclein - metabolism</subject><subject>Amygdala</subject><subject>Amygdala - metabolism</subject><subject>Amygdala - pathology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Avoidance behavior</subject><subject>Behavior</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - pathology</subject><subject>Caspase</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase-3</subject><subject>Cell death</subject><subject>Complications</subject><subject>Creatine</subject><subject>Disease Models, Animal</subject><subject>Glial fibrillary acidic protein</subject><subject>Gliosis</subject><subject>Gliosis - metabolism</subject><subject>Gliosis - pathology</subject><subject>Glycine</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Humanities and Social Sciences</subject><subject>Inositol</subject><subject>Long-term effects</subject><subject>Male</subject><subject>Memory, Short-Term - physiology</subject><subject>Microglia</subject><subject>multidisciplinary</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative Diseases - metabolism</subject><subject>Neurodegenerative Diseases - pathology</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Nucleus accumbens</subject><subject>Nucleus Accumbens - metabolism</subject><subject>Nucleus Accumbens - pathology</subject><subject>Prefrontal cortex</subject><subject>Prefrontal Cortex - metabolism</subject><subject>Prefrontal Cortex - pathology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Science</subject><subject>Short term memory</subject><subject>Synuclein</subject><subject>Tau protein</subject><subject>Temporal lobe</subject><subject>Traumatic brain injury</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNplkUtLJDEUhYPMoKIu_ANDYDY6UJpHpZLaCEPjPECYjS4lpPJo01QlZVI10P_eNN02PU42N7n57skhB4BLjG4wouI2Jztihjg7AqcE1awilJBPB_sTcJHzCpXFSFvj9hickIZRjlFzCp7vg5mTD0torPPaTxn6AAc7xLSGKhgY7JxiUD0c1fQS-7gsbTfZBLte5anyZVxbA6ek5kFNXsMuqaLgw2pO63Pw2ak-24tdPQNPP-4fF7-qhz8_fy--P1SaoXqqtHbGibZmitCOYt5Qro1xjgnMFWUt7wR2hmjCGkVMXVNhuNGttc5y1ZTzGbjb6o5zN1ijbSh-ejkmP6i0llF5-e9N8C9yGf_KuqGUiY3A1U4gxdfZ5kkOPmvb9yrYOGeJebElcENYQb9-QFdxTuWHCiXaViAi2qZQ11tKp5hLRG5vBiO5yU3ucyvsl0P3e_I9pQJ82wJ53ERl08GT_6m9AXswo9Y</recordid><startdate>20151105</startdate><enddate>20151105</enddate><creator>Sajja, Venkata Siva Sai Sujith</creator><creator>Hubbard, W. 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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 (<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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