1
40
2
-
Text
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URL Address
<a href="http://doi.org/10.1186/s13041-018-0376-5" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s13041-018-0376-5</a>
Pages
34–34
Issue
1
Volume
11
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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RNAseq analysis of hippocampal microglia after kainic acid-induced seizures.
Publisher
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Molecular brain
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-06
Subject
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Animals; Gene Expression Profiling; Gene Ontology; Hippocampus/*pathology; Immunity; Interferon-beta/metabolism; Kainic Acid; Mice; Microglia/*metabolism/*pathology; RNA/*methods; Seizures/*chemically induced; Sequence Analysis; Signal Transduction/genetics; Up-Regulation/genetics
Creator
An entity primarily responsible for making the resource
Bosco Dale B; Zheng Jiaying; Xu Zhiyan; Peng Jiyun; Eyo Ukpong B; Tang Ke; Yan Cheng; Huang Jun; Feng Lijie; Wu Gongxiong; Richardson Jason R; Wang Hui; Wu Long-Jun
Description
An account of the resource
Microglia have been shown to be of critical importance to the progression of temporal lobe epilepsy. However, the broad transcriptional changes that these cells undergo following seizure induction is not well understood. As such, we utilized RNAseq analysis upon microglia isolated from the hippocampus to determine expression pattern alterations following kainic acid induced seizure. We determined that microglia undergo dramatic changes to their expression patterns, particularly with regard to mitochondrial activity and metabolism. We also observed that microglia initiate immunological activity, specifically increasing interferon beta responsiveness. Our results provide novel insights into microglia transcriptional regulation following acute seizures and suggest potential therapeutic targets specifically in microglia for the treatment of seizures and epilepsy.
Identifier
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<a href="http://doi.org/10.1186/s13041-018-0376-5" target="_blank" rel="noreferrer noopener">10.1186/s13041-018-0376-5</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2018
Animals
Bosco Dale B
Department of Pharmaceutical Sciences
Eyo Ukpong B
Feng Lijie
Gene Expression Profiling
Gene Ontology
Hippocampus/*pathology
Huang Jun
Immunity
Interferon-beta/metabolism
Kainic Acid
Mice
Microglia/*metabolism/*pathology
Molecular brain
NEOMED College of Pharmacy
Peng Jiyun
Richardson Jason R
RNA/*methods
Seizures/*chemically induced
Sequence Analysis
Signal Transduction/genetics
Tang Ke
Up-Regulation/genetics
Wang Hui
Wu Gongxiong
Wu Long-Jun
Xu Zhiyan
Yan Cheng
Zheng Jiaying
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.neuro.2016.03.023" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.neuro.2016.03.023</a>
Pages
72–80
Volume
54
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Trimethyltin intoxication induces the migration of ventricular/subventricular zone cells to the injured murine hippocampus.
Publisher
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Neurotoxicology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-05
Subject
The topic of the resource
*Brain injury; *Hippocampus; *Neural stem cells; *Neurogenesis; *Subventricular stem cells; *Trimethyltin; Amino Acids/metabolism; Animals; Brain Injuries/*pathology; Bromodeoxyuridine/metabolism; Cell Movement/*drug effects; Functional Laterality; Glial Fibrillary Acidic Protein/metabolism; Hippocampus/*pathology; Inbred C3H; Lateral Ventricles/drug effects/*pathology; Male; Mice; Neurogenesis/drug effects/physiology; Trimethyltin Compounds/*toxicity
Creator
An entity primarily responsible for making the resource
Weig Blair C; Richardson Jason R; Lowndes Herbert E; Reuhl Kenneth R
Description
An account of the resource
Following the postnatal decline of cell proliferation in the mammalian central nervous system, the adult brain retains progenitor cells with stem cell-like properties in the subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampus. Brain injury can stimulate proliferation and redirect the migration pattern of SVZ precursor cells to the injury site. Sublethal exposure to the neurotoxicant trimethyltin (TMT) causes dose-dependent necrosis and apoptosis in the hippocampus dentate gyrus and increases SGZ stem cell proliferation to generate new granule cells. To determine whether SVZ cells also contribute to the repopulation of the TMT-damaged dentate gyrus, 6-8 week old male C3H mice were injected with the carbocyanine dye spDiI and bromodeoxyuridine (80mg/kg; ip.) to label ventricular cells prior to TMT exposure. The presence of labeled cells in hippocampus was determined 7 and 28days after TMT exposure. No significant change in the number of BrdU(+) and spDiI(+) cells was observed in the dentate gyrus 7days after TMT treatment. However, 28days after TMT treatment there was a 3-4 fold increase in the number of spDiI-labeled cells in the hippocampal hilus and dentate gyrus. Few spDiI(+) cells stained positive for the mature phenotypic markers NeuN or GFAP, suggesting they may represent undifferentiated cells. A small percentage of migrating cells were BrdU(+)/spDiI(+), indicating some newly produced, SVZ- derived precursors migrated to the hippocampus. Taken together, these data suggest that TMT-induced injury of the hippocampus can stimulate the migration of ventricular zone-derived cells to injured dentate gyrus.
Identifier
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<a href="http://doi.org/10.1016/j.neuro.2016.03.023" target="_blank" rel="noreferrer noopener">10.1016/j.neuro.2016.03.023</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Brain injury
*Hippocampus
*Neural stem cells
*Neurogenesis
*Subventricular stem cells
*Trimethyltin
2016
Amino Acids/metabolism
Animals
Brain Injuries/*pathology
Bromodeoxyuridine/metabolism
Cell Movement/*drug effects
Department of Pharmaceutical Sciences
Functional Laterality
Glial Fibrillary Acidic Protein/metabolism
Hippocampus/*pathology
Inbred C3H
Lateral Ventricles/drug effects/*pathology
Lowndes Herbert E
Male
Mice
NEOMED College of Pharmacy
Neurogenesis/drug effects/physiology
Neurotoxicology
Reuhl Kenneth R
Richardson Jason R
Trimethyltin Compounds/*toxicity
Weig Blair C