Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation.
Identifieur interne : 000C83 ( Main/Corpus ); précédent : 000C82; suivant : 000C84Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation.
Auteurs : Martine Liberge ; Christine Manrique ; Laurence Bernard-Demanze ; Michel LacourSource :
- Journal of neuroinflammation [ 1742-2094 ] ; 2010.
English descriptors
- KwdEn :
- Animals (MeSH), Behavior, Animal (physiology), Biomarkers (metabolism), Inflammation (metabolism), Inflammation (pathology), Male (MeSH), NF-kappa B (metabolism), Posture (MeSH), Rats (MeSH), Rats, Long-Evans (MeSH), Superoxide Dismutase (metabolism), Tumor Necrosis Factor-alpha (metabolism), Vestibular Nerve (pathology), Vestibular Nerve (surgery), Vestibular Nuclei (cytology), Vestibular Nuclei (metabolism), Vestibular Nuclei (pathology).
- MESH :
- chemical , metabolism : Biomarkers, NF-kappa B, Superoxide Dismutase, Tumor Necrosis Factor-alpha.
- cytology : Vestibular Nuclei.
- metabolism : Inflammation, Vestibular Nuclei.
- pathology : Inflammation, Vestibular Nerve, Vestibular Nuclei.
- physiology : Behavior, Animal.
- surgery : Vestibular Nerve.
- Animals, Male, Posture, Rats, Rats, Long-Evans.
Abstract
BACKGROUND
Unilateral vestibular deafferentation results in strong microglial and astroglial activation in the vestibular nuclei (VN) that could be due to an inflammatory response. This study was aimed at determining if markers of inflammation are upregulated in the VN after chemical unilateral labyrinthectomy (UL) in the rat, and if the inflammatory response, if any, induces the expression of neuroprotective factors that could promote the plasticity mechanisms involved in the vestibular compensation process. The expressions of inflammatory and neuroprotective factors after chemical or mechanical UL were also compared to verify that the inflammatory response was not due to the toxicity of sodium arsanilate.
METHODS
Immunohistological investigations combined the labeling of tumor necrosis factor α (TNFα), as a marker of the VN inflammatory response, and of nuclear transcription factor κB (NFκB) and manganese superoxide dismutase (MnSOD), as markers of neuroprotection that could be expressed in the VN because of inflammation. Immunoreactivity (Ir) of the VN cells was quantified in the VN complex of rats. Behavioral investigations were performed to assess the functional recovery process, including both static (support surface) and dynamic (air-righting and landing reflexes) postural tests.
RESULTS
Chemical UL (arsanilate transtympanic injection) induced a significant increase in the number of TNFα-Ir cells in the medial and inferior VN on both sides. These changes were detectable as early as 4 h after vestibular lesion, persisted at 1 day, and regained nearly normal values at 3 days. The early increase in TNFα expression was followed by a slightly delayed upregulation of NFκB 8 h after chemical UL, peaking at 1 day, and regaining control values 3 days later. By contrast, upregulation of MnSOD was more strongly delayed (1 day), with a peak at 3 days, and a return to control values at 15 days. Similar changes of TNFα, NFκB, and MnSOD expression were found in rats submitted to mechanical UL. Behavioral observations showed strong posturo-locomotor deficits early after chemical UL (1 day) and a complete functional recovery 6 weeks later.
CONCLUSIONS
Our results suggest that the upregulation of inflammatory and neuroprotective factors after vestibular deafferentation in the VN may constitute a favorable neuronal environment for the vestibular compensation process.
DOI: 10.1186/1742-2094-7-91
PubMed: 21143912
PubMed Central: PMC3004876
Links to Exploration step
pubmed:21143912Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation.</title><author><name sortKey="Liberge, Martine" sort="Liberge, Martine" uniqKey="Liberge M" first="Martine" last="Liberge">Martine Liberge</name><affiliation><nlm:affiliation>Université Aix-Marseille, UMR 6149 Université de Provence/CNRS, Neurobiologie Intégrative et Adaptative, Pôle 3C, Comportement, Cerveau, Cognition, Centre de St Charles, Case B, 3 Place Victor Hugo, 13331 Marseille Cedex 3, France. martine.liberge@univ-provence.fr</nlm:affiliation></affiliation></author><author><name sortKey="Manrique, Christine" sort="Manrique, Christine" uniqKey="Manrique C" first="Christine" last="Manrique">Christine Manrique</name></author><author><name sortKey="Bernard Demanze, Laurence" sort="Bernard Demanze, Laurence" uniqKey="Bernard Demanze L" first="Laurence" last="Bernard-Demanze">Laurence Bernard-Demanze</name></author><author><name sortKey="Lacour, Michel" sort="Lacour, Michel" uniqKey="Lacour M" first="Michel" last="Lacour">Michel Lacour</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:21143912</idno><idno type="pmid">21143912</idno><idno type="doi">10.1186/1742-2094-7-91</idno><idno type="pmc">PMC3004876</idno><idno type="wicri:Area/Main/Corpus">000C83</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000C83</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation.</title><author><name sortKey="Liberge, Martine" sort="Liberge, Martine" uniqKey="Liberge M" first="Martine" last="Liberge">Martine Liberge</name><affiliation><nlm:affiliation>Université Aix-Marseille, UMR 6149 Université de Provence/CNRS, Neurobiologie Intégrative et Adaptative, Pôle 3C, Comportement, Cerveau, Cognition, Centre de St Charles, Case B, 3 Place Victor Hugo, 13331 Marseille Cedex 3, France. martine.liberge@univ-provence.fr</nlm:affiliation></affiliation></author><author><name sortKey="Manrique, Christine" sort="Manrique, Christine" uniqKey="Manrique C" first="Christine" last="Manrique">Christine Manrique</name></author><author><name sortKey="Bernard Demanze, Laurence" sort="Bernard Demanze, Laurence" uniqKey="Bernard Demanze L" first="Laurence" last="Bernard-Demanze">Laurence Bernard-Demanze</name></author><author><name sortKey="Lacour, Michel" sort="Lacour, Michel" uniqKey="Lacour M" first="Michel" last="Lacour">Michel Lacour</name></author></analytic><series><title level="j">Journal of neuroinflammation</title><idno type="eISSN">1742-2094</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Behavior, Animal (physiology)</term><term>Biomarkers (metabolism)</term><term>Inflammation (metabolism)</term><term>Inflammation (pathology)</term><term>Male (MeSH)</term><term>NF-kappa B (metabolism)</term><term>Posture (MeSH)</term><term>Rats (MeSH)</term><term>Rats, Long-Evans (MeSH)</term><term>Superoxide Dismutase (metabolism)</term><term>Tumor Necrosis Factor-alpha (metabolism)</term><term>Vestibular Nerve (pathology)</term><term>Vestibular Nerve (surgery)</term><term>Vestibular Nuclei (cytology)</term><term>Vestibular Nuclei (metabolism)</term><term>Vestibular Nuclei (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers</term><term>NF-kappa B</term><term>Superoxide Dismutase</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Vestibular Nuclei</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Inflammation</term><term>Vestibular Nuclei</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term><term>Vestibular Nerve</term><term>Vestibular Nuclei</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Behavior, Animal</term></keywords><keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Vestibular Nerve</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Male</term><term>Posture</term><term>Rats</term><term>Rats, Long-Evans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b></p><p>Unilateral vestibular deafferentation results in strong microglial and astroglial activation in the vestibular nuclei (VN) that could be due to an inflammatory response. This study was aimed at determining if markers of inflammation are upregulated in the VN after chemical unilateral labyrinthectomy (UL) in the rat, and if the inflammatory response, if any, induces the expression of neuroprotective factors that could promote the plasticity mechanisms involved in the vestibular compensation process. The expressions of inflammatory and neuroprotective factors after chemical or mechanical UL were also compared to verify that the inflammatory response was not due to the toxicity of sodium arsanilate.</p></div><div type="abstract" xml:lang="en"><p><b>METHODS</b></p><p>Immunohistological investigations combined the labeling of tumor necrosis factor α (TNFα), as a marker of the VN inflammatory response, and of nuclear transcription factor κB (NFκB) and manganese superoxide dismutase (MnSOD), as markers of neuroprotection that could be expressed in the VN because of inflammation. Immunoreactivity (Ir) of the VN cells was quantified in the VN complex of rats. Behavioral investigations were performed to assess the functional recovery process, including both static (support surface) and dynamic (air-righting and landing reflexes) postural tests.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>Chemical UL (arsanilate transtympanic injection) induced a significant increase in the number of TNFα-Ir cells in the medial and inferior VN on both sides. These changes were detectable as early as 4 h after vestibular lesion, persisted at 1 day, and regained nearly normal values at 3 days. The early increase in TNFα expression was followed by a slightly delayed upregulation of NFκB 8 h after chemical UL, peaking at 1 day, and regaining control values 3 days later. By contrast, upregulation of MnSOD was more strongly delayed (1 day), with a peak at 3 days, and a return to control values at 15 days. Similar changes of TNFα, NFκB, and MnSOD expression were found in rats submitted to mechanical UL. Behavioral observations showed strong posturo-locomotor deficits early after chemical UL (1 day) and a complete functional recovery 6 weeks later.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>Our results suggest that the upregulation of inflammatory and neuroprotective factors after vestibular deafferentation in the VN may constitute a favorable neuronal environment for the vestibular compensation process.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21143912</PMID><DateCompleted><Year>2011</Year><Month>04</Month><Day>12</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1742-2094</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><PubDate><Year>2010</Year><Month>Dec</Month><Day>09</Day></PubDate></JournalIssue><Title>Journal of neuroinflammation</Title><ISOAbbreviation>J Neuroinflammation</ISOAbbreviation></Journal><ArticleTitle>Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation.</ArticleTitle><Pagination><MedlinePgn>91</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/1742-2094-7-91</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Unilateral vestibular deafferentation results in strong microglial and astroglial activation in the vestibular nuclei (VN) that could be due to an inflammatory response. This study was aimed at determining if markers of inflammation are upregulated in the VN after chemical unilateral labyrinthectomy (UL) in the rat, and if the inflammatory response, if any, induces the expression of neuroprotective factors that could promote the plasticity mechanisms involved in the vestibular compensation process. The expressions of inflammatory and neuroprotective factors after chemical or mechanical UL were also compared to verify that the inflammatory response was not due to the toxicity of sodium arsanilate.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Immunohistological investigations combined the labeling of tumor necrosis factor α (TNFα), as a marker of the VN inflammatory response, and of nuclear transcription factor κB (NFκB) and manganese superoxide dismutase (MnSOD), as markers of neuroprotection that could be expressed in the VN because of inflammation. Immunoreactivity (Ir) of the VN cells was quantified in the VN complex of rats. Behavioral investigations were performed to assess the functional recovery process, including both static (support surface) and dynamic (air-righting and landing reflexes) postural tests.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Chemical UL (arsanilate transtympanic injection) induced a significant increase in the number of TNFα-Ir cells in the medial and inferior VN on both sides. These changes were detectable as early as 4 h after vestibular lesion, persisted at 1 day, and regained nearly normal values at 3 days. The early increase in TNFα expression was followed by a slightly delayed upregulation of NFκB 8 h after chemical UL, peaking at 1 day, and regaining control values 3 days later. By contrast, upregulation of MnSOD was more strongly delayed (1 day), with a peak at 3 days, and a return to control values at 15 days. Similar changes of TNFα, NFκB, and MnSOD expression were found in rats submitted to mechanical UL. Behavioral observations showed strong posturo-locomotor deficits early after chemical UL (1 day) and a complete functional recovery 6 weeks later.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our results suggest that the upregulation of inflammatory and neuroprotective factors after vestibular deafferentation in the VN may constitute a favorable neuronal environment for the vestibular compensation process.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Liberge</LastName><ForeName>Martine</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Université Aix-Marseille, UMR 6149 Université de Provence/CNRS, Neurobiologie Intégrative et Adaptative, Pôle 3C, Comportement, Cerveau, Cognition, Centre de St Charles, Case B, 3 Place Victor Hugo, 13331 Marseille Cedex 3, France. martine.liberge@univ-provence.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Manrique</LastName><ForeName>Christine</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Bernard-Demanze</LastName><ForeName>Laurence</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Lacour</LastName><ForeName>Michel</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>12</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neuroinflammation</MedlineTA><NlmUniqueID>101222974</NlmUniqueID><ISSNLinking>1742-2094</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001522" MajorTopicYN="N">Behavior, Animal</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011187" MajorTopicYN="N">Posture</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020318" MajorTopicYN="N">Rats, Long-Evans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014725" MajorTopicYN="N">Vestibular Nerve</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="N">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014726" MajorTopicYN="N">Vestibular Nuclei</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>07</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2010</Year><Month>12</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>4</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">21143912</ArticleId><ArticleId IdType="pii">1742-2094-7-91</ArticleId><ArticleId IdType="doi">10.1186/1742-2094-7-91</ArticleId><ArticleId IdType="pmc">PMC3004876</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>J Neurosci. 2001 Sep 1;21(17):6617-25</Citation><ArticleIdList><ArticleId IdType="pubmed">11517251</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Microbiol Rev. 2001 Oct;14(4):810-20, table of contents</Citation><ArticleIdList><ArticleId IdType="pubmed">11585786</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Hum Reprod. 2001 Nov;7(11):1065-72</Citation><ArticleIdList><ArticleId IdType="pubmed">11675473</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Neurosci. 2001 Nov;4(11):1116-22</Citation><ArticleIdList><ArticleId IdType="pubmed">11600888</ArticleId></ArticleIdList></Reference><Reference><Citation>Neurobiol Aging. 2001 Nov-Dec;22(6):873-83</Citation><ArticleIdList><ArticleId IdType="pubmed">11754994</ArticleId></ArticleIdList></Reference><Reference><Citation>Neurosci Lett. 2002 Feb 8;319(1):9-12</Citation><ArticleIdList><ArticleId IdType="pubmed">11814641</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 2002 Apr 1;22(7):RC216</Citation><ArticleIdList><ArticleId IdType="pubmed">11917000</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 2002 Apr 15;22(8):3025-32</Citation><ArticleIdList><ArticleId IdType="pubmed">11943805</ArticleId></ArticleIdList></Reference><Reference><Citation>Oncogene. 2002 May 30;21(24):3917-24</Citation><ArticleIdList><ArticleId IdType="pubmed">12032830</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci Res. 2004 May 15;76(4):466-74</Citation><ArticleIdList><ArticleId IdType="pubmed">15114618</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2004 Jul 30;279(31):32869-81</Citation><ArticleIdList><ArticleId IdType="pubmed">15155767</ArticleId></ArticleIdList></Reference><Reference><Citation>Clin Microbiol Rev. 2004 Oct;17(4):942-64, table of contents</Citation><ArticleIdList><ArticleId IdType="pubmed">15489356</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurophysiol. 1966 May;29(3):467-92</Citation><ArticleIdList><ArticleId IdType="pubmed">5961161</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurophysiol. 1968 Mar;31(2):176-85</Citation><ArticleIdList><ArticleId IdType="pubmed">5687381</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1973 Jul 10;248(13):4793-6</Citation><ArticleIdList><ArticleId IdType="pubmed">4578091</ArticleId></ArticleIdList></Reference><Reference><Citation>Acta Otolaryngol. 1977 May-Jun;83(5-6):429-40</Citation><ArticleIdList><ArticleId IdType="pubmed">888679</ArticleId></ArticleIdList></Reference><Reference><Citation>Arch Ital Biol. 1978 Jun;116(2):130-72</Citation><ArticleIdList><ArticleId IdType="pubmed">80203</ArticleId></ArticleIdList></Reference><Reference><Citation>Ann Otol Rhinol Laryngol Suppl. 1982 Sep-Oct;97:16-32</Citation><ArticleIdList><ArticleId IdType="pubmed">6814326</ArticleId></ArticleIdList></Reference><Reference><Citation>Brain Res. 1984 Jun 8;302(2):245-56</Citation><ArticleIdList><ArticleId IdType="pubmed">6610459</ArticleId></ArticleIdList></Reference><Reference><Citation>Physiol Behav. 1986;37(5):805-14</Citation><ArticleIdList><ArticleId IdType="pubmed">2877470</ArticleId></ArticleIdList></Reference><Reference><Citation>Brain Res Brain Res Rev. 1989 Apr-Jun;14(2):155-80</Citation><ArticleIdList><ArticleId IdType="pubmed">2665890</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1990 Feb 15;265(5):2856-64</Citation><ArticleIdList><ArticleId IdType="pubmed">2406241</ArticleId></ArticleIdList></Reference><Reference><Citation>J Immunol. 1991 Jul 1;147(1):149-54</Citation><ArticleIdList><ArticleId IdType="pubmed">1904900</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 1992 Nov;12(11):4489-500</Citation><ArticleIdList><ArticleId IdType="pubmed">1432106</ArticleId></ArticleIdList></Reference><Reference><Citation>Free Radic Biol Med. 1994 Sep;17(3):235-48</Citation><ArticleIdList><ArticleId IdType="pubmed">7982629</ArticleId></ArticleIdList></Reference><Reference><Citation>J Acquir Immune Defic Syndr Hum Retrovirol. 1995 Aug 1;9(4):379-88</Citation><ArticleIdList><ArticleId IdType="pubmed">7600105</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 1995 Jul 1;9(13):1586-97</Citation><ArticleIdList><ArticleId IdType="pubmed">7628694</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9328-32</Citation><ArticleIdList><ArticleId IdType="pubmed">7568127</ArticleId></ArticleIdList></Reference><Reference><Citation>Prog Neurobiol. 1995 Jun;46(2-3):97-129</Citation><ArticleIdList><ArticleId IdType="pubmed">7568917</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurophysiol. 1995 Nov;74(5):2087-99</Citation><ArticleIdList><ArticleId IdType="pubmed">8592199</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurochem. 1996 Feb;66(2):869-72</Citation><ArticleIdList><ArticleId IdType="pubmed">8592164</ArticleId></ArticleIdList></Reference><Reference><Citation>Neuroscience. 1996 Jan;70(2):515-46</Citation><ArticleIdList><ArticleId IdType="pubmed">8848156</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Med. 1996 Jul;2(7):788-94</Citation><ArticleIdList><ArticleId IdType="pubmed">8673925</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1997 Feb 7;272(6):3550-3</Citation><ArticleIdList><ArticleId IdType="pubmed">9013604</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2642-7</Citation><ArticleIdList><ArticleId IdType="pubmed">9122249</ArticleId></ArticleIdList></Reference><Reference><Citation>Stroke. 1997 May;28(5):1073-80; discussion 1080-1</Citation><ArticleIdList><ArticleId IdType="pubmed">9158652</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci Res. 1997 Sep 15;49(6):681-97</Citation><ArticleIdList><ArticleId IdType="pubmed">9335256</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 1997 Dec;17(12):6970-81</Citation><ArticleIdList><ArticleId IdType="pubmed">9372929</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 1998 Jan 15;18(2):687-97</Citation><ArticleIdList><ArticleId IdType="pubmed">9425011</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 1998 Mar 15;18(6):2040-55</Citation><ArticleIdList><ArticleId IdType="pubmed">9482791</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 1998 May 22;273(21):13245-54</Citation><ArticleIdList><ArticleId IdType="pubmed">9582369</ArticleId></ArticleIdList></Reference><Reference><Citation>Brain Res Mol Brain Res. 1998 Aug 31;59(2):135-42</Citation><ArticleIdList><ArticleId IdType="pubmed">9729336</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur J Neurosci. 1998 Oct;10(10):3115-26</Citation><ArticleIdList><ArticleId IdType="pubmed">9786206</ArticleId></ArticleIdList></Reference><Reference><Citation>Ann Otol Rhinol Laryngol. 1999 Feb;108(2):181-8</Citation><ArticleIdList><ArticleId IdType="pubmed">10030238</ArticleId></ArticleIdList></Reference><Reference><Citation>Brain Res. 1999 Feb 20;819(1-2):170-3</Citation><ArticleIdList><ArticleId IdType="pubmed">10082875</ArticleId></ArticleIdList></Reference><Reference><Citation>Brain Res. 1999 Apr 3;824(1):1-17</Citation><ArticleIdList><ArticleId IdType="pubmed">10095037</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neuroimmunol. 1999 Jan 1;93(1-2):53-71</Citation><ArticleIdList><ArticleId IdType="pubmed">10378869</ArticleId></ArticleIdList></Reference><Reference><Citation>Brain Res Brain Res Rev. 1999 Jul;30(1):77-105</Citation><ArticleIdList><ArticleId IdType="pubmed">10407127</ArticleId></ArticleIdList></Reference><Reference><Citation>Neuroscience. 1999;92(4):1475-90</Citation><ArticleIdList><ArticleId IdType="pubmed">10426501</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):9409-14</Citation><ArticleIdList><ArticleId IdType="pubmed">10430956</ArticleId></ArticleIdList></Reference><Reference><Citation>DNA Cell Biol. 1999 Sep;18(9):709-22</Citation><ArticleIdList><ArticleId IdType="pubmed">10492402</ArticleId></ArticleIdList></Reference><Reference><Citation>Acta Neurochir Suppl. 1999;73:21-30</Citation><ArticleIdList><ArticleId IdType="pubmed">10494337</ArticleId></ArticleIdList></Reference><Reference><Citation>Neuroscience. 2005;130(4):853-65</Citation><ArticleIdList><ArticleId IdType="pubmed">15652984</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurotrauma. 2004 Dec;21(12):1778-94</Citation><ArticleIdList><ArticleId IdType="pubmed">15684769</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 2006 Jan 4;26(1):143-51</Citation><ArticleIdList><ArticleId IdType="pubmed">16399681</ArticleId></ArticleIdList></Reference><Reference><Citation>BMC Neurosci. 2006;7:64</Citation><ArticleIdList><ArticleId IdType="pubmed">16987412</ArticleId></ArticleIdList></Reference><Reference><Citation>J Mol Neurosci. 2006;29(3):279-88</Citation><ArticleIdList><ArticleId IdType="pubmed">17085785</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur J Neurosci. 2007 Jan;25(1):47-58</Citation><ArticleIdList><ArticleId IdType="pubmed">17241266</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 2007 Mar 28;27(13):3503-11</Citation><ArticleIdList><ArticleId IdType="pubmed">17392466</ArticleId></ArticleIdList></Reference><Reference><Citation>J Alzheimers Dis. 2008 Mar;13(2):111-22</Citation><ArticleIdList><ArticleId IdType="pubmed">18376053</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 2008 Apr 9;28(15):3911-9</Citation><ArticleIdList><ArticleId IdType="pubmed">18400889</ArticleId></ArticleIdList></Reference><Reference><Citation>Stem Cells. 2008 Sep;26(9):2361-71</Citation><ArticleIdList><ArticleId IdType="pubmed">18583543</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurochem. 2008 Nov;107(4):1158-67</Citation><ArticleIdList><ArticleId IdType="pubmed">18823372</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 2009 Feb 4;29(5):1319-30</Citation><ArticleIdList><ArticleId IdType="pubmed">19193879</ArticleId></ArticleIdList></Reference><Reference><Citation>Ann N Y Acad Sci. 2009 May;1164:268-78</Citation><ArticleIdList><ArticleId IdType="pubmed">19645911</ArticleId></ArticleIdList></Reference><Reference><Citation>Neuroscience. 2009 Dec 29;164(4):1444-56</Citation><ArticleIdList><ArticleId IdType="pubmed">19782724</ArticleId></ArticleIdList></Reference><Reference><Citation>Restor Neurol Neurosci. 2010;28(1):19-35</Citation><ArticleIdList><ArticleId IdType="pubmed">20086280</ArticleId></ArticleIdList></Reference><Reference><Citation>Synapse. 2000 Feb;35(2):151-9</Citation><ArticleIdList><ArticleId IdType="pubmed">10611641</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurochem. 2000 Feb;74(2):457-71</Citation><ArticleIdList><ArticleId IdType="pubmed">10646496</ArticleId></ArticleIdList></Reference><Reference><Citation>Cytokine Growth Factor Rev. 1999 Jun;10(2):119-30</Citation><ArticleIdList><ArticleId IdType="pubmed">10743503</ArticleId></ArticleIdList></Reference><Reference><Citation>Prog Neurobiol. 2000 Oct;62(3):313-25</Citation><ArticleIdList><ArticleId IdType="pubmed">10840152</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 2000 Oct 15;20(20):7556-63</Citation><ArticleIdList><ArticleId IdType="pubmed">11027214</ArticleId></ArticleIdList></Reference><Reference><Citation>J Exp Med. 2001 Feb 19;193(4):427-34</Citation><ArticleIdList><ArticleId IdType="pubmed">11181695</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 2001 Mar 15;21(6):2058-66</Citation><ArticleIdList><ArticleId IdType="pubmed">11245689</ArticleId></ArticleIdList></Reference><Reference><Citation>Eur J Neurosci. 2001 Jun;13(12):2255-67</Citation><ArticleIdList><ArticleId IdType="pubmed">11454029</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/PosturoV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000C83 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000C83 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= PosturoV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= pubmed:21143912
|texte= Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Corpus/RBID.i -Sk "pubmed:21143912" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a PosturoV1
| This area was generated with Dilib version V0.6.37. |  |