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We are analyzing https://link.springer.com/article/10.1007/s12031-015-0626-2.

Title:
Acute Response of the Hippocampal Transcriptome Following Mild Traumatic Brain Injury After Controlled Cortical Impact in the Rat | Journal of Molecular Neuroscience
Description:
We have previously demonstrated that mild controlled cortical impact (mCCI) injury to rat cortex causes indirect, concussive injury to underlying hippocampus and other brain regions, providing a reproducible model for mild traumatic brain injury (mTBI) and its neurochemical, synaptic, and behavioral sequelae. Here, we extend a preliminary gene expression study of the hippocampus-specific events occurring after mCCI and identify 193 transcripts significantly upregulated, and 21 transcripts significantly downregulated, 24 h after mCCI. Fifty-three percent of genes altered by mCCI within 24 h of injury are predicted to be expressed only in the non-neuronal/glial cellular compartment, with only 13 % predicted to be expressed only in neurons. The set of upregulated genes following mCCI was interrogated using Ingenuity Pathway Analysis (IPA) augmented with manual curation of the literature (190 transcripts accepted for analysis), revealing a core group of 15 first messengers, mostly inflammatory cytokines, predicted to account for >99 % of the transcript upregulation occurring 24 h after mCCI. Convergent analysis of predicted transcription factors (TFs) regulating the mCCI target genes, carried out in IPA relative to the entire Affymetrix-curated transcriptome, revealed a high concordance with TFs regulated by the cohort of 15 cytokines/cytokine-like messengers independently accounting for upregulation of the mCCI transcript cohort. TFs predicted to regulate transcription of the 193-gene mCCI cohort also displayed a high degree of overlap with TFs predicted to regulate glia-, rather than neuron-specific genes in cortical tissue. We conclude that mCCI predominantly affects transcription of non-neuronal genes within the first 24 h after insult. This finding suggests that early non-neuronal events trigger later permanent neuronal changes after mTBI, and that early intervention after mTBI could potentially affect the neurochemical cascade leading to later reported synaptic and behavioral dysfunction.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
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Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

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Traffic Estimate {📈}

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,016 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

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Keywords {🔍}

pubmed, article, google, scholar, injury, brain, traumatic, cas, mild, eiden, central, analysis, cortical, mcci, samal, genes, controlled, impact, expression, access, usa, almeidasuhett, marini, braga, gene, predicted, res, privacy, cookies, content, data, journal, research, hippocampal, rat, model, transcription, bethesda, publish, search, molecular, neuroscience, response, mtbi, behavioral, ipa, tfs, cohort, open, july,

Topics {✒️}

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Schema {🗺️}

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      mainEntity:
         headline:Acute Response of the Hippocampal Transcriptome Following Mild Traumatic Brain Injury After Controlled Cortical Impact in the Rat
         description:We have previously demonstrated that mild controlled cortical impact (mCCI) injury to rat cortex causes indirect, concussive injury to underlying hippocampus and other brain regions, providing a reproducible model for mild traumatic brain injury (mTBI) and its neurochemical, synaptic, and behavioral sequelae. Here, we extend a preliminary gene expression study of the hippocampus-specific events occurring after mCCI and identify 193 transcripts significantly upregulated, and 21 transcripts significantly downregulated, 24 h after mCCI. Fifty-three percent of genes altered by mCCI within 24 h of injury are predicted to be expressed only in the non-neuronal/glial cellular compartment, with only 13 % predicted to be expressed only in neurons. The set of upregulated genes following mCCI was interrogated using Ingenuity Pathway Analysis (IPA) augmented with manual curation of the literature (190 transcripts accepted for analysis), revealing a core group of 15 first messengers, mostly inflammatory cytokines, predicted to account for >99 % of the transcript upregulation occurring 24 h after mCCI. Convergent analysis of predicted transcription factors (TFs) regulating the mCCI target genes, carried out in IPA relative to the entire Affymetrix-curated transcriptome, revealed a high concordance with TFs regulated by the cohort of 15 cytokines/cytokine-like messengers independently accounting for upregulation of the mCCI transcript cohort. TFs predicted to regulate transcription of the 193-gene mCCI cohort also displayed a high degree of overlap with TFs predicted to regulate glia-, rather than neuron-specific genes in cortical tissue. We conclude that mCCI predominantly affects transcription of non-neuronal genes within the first 24 h after insult. This finding suggests that early non-neuronal events trigger later permanent neuronal changes after mTBI, and that early intervention after mTBI could potentially affect the neurochemical cascade leading to later reported synaptic and behavioral dysfunction.
         datePublished:2015-08-29T00:00:00Z
         dateModified:2015-08-29T00:00:00Z
         pageStart:282
         pageEnd:303
         sameAs:https://doi.org/10.1007/s12031-015-0626-2
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            Controlled cortical impact
            Inflammation
            Mild traumatic brain injury
            Neurosciences
            Neurochemistry
            Cell Biology
            Proteomics
            Neurology
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      headline:Acute Response of the Hippocampal Transcriptome Following Mild Traumatic Brain Injury After Controlled Cortical Impact in the Rat
      description:We have previously demonstrated that mild controlled cortical impact (mCCI) injury to rat cortex causes indirect, concussive injury to underlying hippocampus and other brain regions, providing a reproducible model for mild traumatic brain injury (mTBI) and its neurochemical, synaptic, and behavioral sequelae. Here, we extend a preliminary gene expression study of the hippocampus-specific events occurring after mCCI and identify 193 transcripts significantly upregulated, and 21 transcripts significantly downregulated, 24 h after mCCI. Fifty-three percent of genes altered by mCCI within 24 h of injury are predicted to be expressed only in the non-neuronal/glial cellular compartment, with only 13 % predicted to be expressed only in neurons. The set of upregulated genes following mCCI was interrogated using Ingenuity Pathway Analysis (IPA) augmented with manual curation of the literature (190 transcripts accepted for analysis), revealing a core group of 15 first messengers, mostly inflammatory cytokines, predicted to account for >99 % of the transcript upregulation occurring 24 h after mCCI. Convergent analysis of predicted transcription factors (TFs) regulating the mCCI target genes, carried out in IPA relative to the entire Affymetrix-curated transcriptome, revealed a high concordance with TFs regulated by the cohort of 15 cytokines/cytokine-like messengers independently accounting for upregulation of the mCCI transcript cohort. TFs predicted to regulate transcription of the 193-gene mCCI cohort also displayed a high degree of overlap with TFs predicted to regulate glia-, rather than neuron-specific genes in cortical tissue. We conclude that mCCI predominantly affects transcription of non-neuronal genes within the first 24 h after insult. This finding suggests that early non-neuronal events trigger later permanent neuronal changes after mTBI, and that early intervention after mTBI could potentially affect the neurochemical cascade leading to later reported synaptic and behavioral dysfunction.
      datePublished:2015-08-29T00:00:00Z
      dateModified:2015-08-29T00:00:00Z
      pageStart:282
      pageEnd:303
      sameAs:https://doi.org/10.1007/s12031-015-0626-2
      keywords:
         Hippocampus
         Controlled cortical impact
         Inflammation
         Mild traumatic brain injury
         Neurosciences
         Neurochemistry
         Cell Biology
         Proteomics
         Neurology
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                  address:
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                     type:PostalAddress
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            name:Cameron K. Waites
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                     name:Department of Neurology, F. Edward Hebert School of Medicine Uniformed Services University of the Health Sciences, Bethesda, USA
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         name:Department of Anatomy, Physiology and Genetics, F. Edward Hebert School of Medicine, Bethesda, USA
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      affiliation:
            name:National Institute of Mental Health
            address:
               name:Section on Molecular Neuroscience, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, Bethesda, USA
               type:PostalAddress
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      name:Cameron K. Waites
      affiliation:
            name:National Institute of Mental Health
            address:
               name:Section on Molecular Neuroscience, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, Bethesda, USA
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            name:F. Edward Hebert School of Medicine
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               name:Department of Anatomy, Physiology and Genetics, F. Edward Hebert School of Medicine, Bethesda, USA
               type:PostalAddress
            type:Organization
      name:Zheng Li
      affiliation:
            name:National Institute of Mental Health
            address:
               name:Unit on Synapse Development and Plasticity, National Institute of Mental Health, Bethesda, USA
               type:PostalAddress
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      name:Ann M. Marini
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            name:F. Edward Hebert School of Medicine Uniformed Services University of the Health Sciences
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               name:Department of Neurology, F. Edward Hebert School of Medicine Uniformed Services University of the Health Sciences, Bethesda, USA
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            name:
            address:
               name:San Diego, USA
               type:PostalAddress
            type:Organization
      name:Abdel Elkahloun
      affiliation:
            name:National Human Genome Research Institute
            address:
               name:Microarray Core, National Human Genome Research Institute, Bethesda, USA
               type:PostalAddress
            type:Organization
      name:Maria F. M. Braga
      affiliation:
            name:F. Edward Hebert School of Medicine
            address:
               name:Department of Anatomy, Physiology and Genetics, F. Edward Hebert School of Medicine, Bethesda, USA
               type:PostalAddress
            type:Organization
      name:Lee E. Eiden
      affiliation:
            name:National Institute of Mental Health
            address:
               name:Section on Molecular Neuroscience, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, Bethesda, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Section on Molecular Neuroscience, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, Bethesda, USA
      name:Section on Molecular Neuroscience, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, Bethesda, USA
      name:Department of Anatomy, Physiology and Genetics, F. Edward Hebert School of Medicine, Bethesda, USA
      name:Unit on Synapse Development and Plasticity, National Institute of Mental Health, Bethesda, USA
      name:Department of Neurology, F. Edward Hebert School of Medicine Uniformed Services University of the Health Sciences, Bethesda, USA
      name:San Diego, USA
      name:Microarray Core, National Human Genome Research Institute, Bethesda, USA
      name:Department of Anatomy, Physiology and Genetics, F. Edward Hebert School of Medicine, Bethesda, USA
      name:Section on Molecular Neuroscience, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, Bethesda, USA
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