Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation.
Identifieur interne : 000C83 ( Main/Curation ); précédent : 000C82; suivant : 000C84Changes in TNFα, NFκB and MnSOD protein in the vestibular nuclei after unilateral vestibular deafferentation.
Auteurs : Martine Liberge [France] ; Christine Manrique ; Laurence Bernard-Demanze ; Michel LacourSource :
- Journal of neuroinflammation [ 1742-2094 ] ; 2010.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Comportement animal (physiologie), Facteur de nécrose tumorale alpha (métabolisme), Facteur de transcription NF-kappa B (métabolisme), Inflammation (anatomopathologie), Inflammation (métabolisme), Marqueurs biologiques (métabolisme), Mâle (MeSH), Nerf vestibulaire (anatomopathologie), Nerf vestibulaire (chirurgie), Noyaux vestibulaires (anatomopathologie), Noyaux vestibulaires (cytologie), Noyaux vestibulaires (métabolisme), Posture (MeSH), Rat Long-Evans (MeSH), Rats (MeSH), Superoxide dismutase (métabolisme).
- MESH :
- anatomopathologie : Inflammation, Nerf vestibulaire, Noyaux vestibulaires.
- chirurgie : Nerf vestibulaire.
- cytologie : Noyaux vestibulaires.
- métabolisme : Facteur de nécrose tumorale alpha, Facteur de transcription NF-kappa B, Inflammation, Marqueurs biologiques, Noyaux vestibulaires, Superoxide dismutase.
- physiologie : Comportement animal.
- Animaux, Mâle, Posture, Rat Long-Evans, Rats.
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
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pubmed:21143912Le document en format XML
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<term>Inflammation (pathology)</term>
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<term>Superoxide Dismutase (metabolism)</term>
<term>Tumor Necrosis Factor-alpha (metabolism)</term>
<term>Vestibular Nerve (pathology)</term>
<term>Vestibular Nerve (surgery)</term>
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<term>Facteur de transcription NF-kappa B (métabolisme)</term>
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<term>Nerf vestibulaire (chirurgie)</term>
<term>Noyaux vestibulaires (anatomopathologie)</term>
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<term>Noyaux vestibulaires (métabolisme)</term>
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<term>Marqueurs biologiques</term>
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<term>Superoxide dismutase</term>
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<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>
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<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>
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