Synaptic Activity Protects Neurons Against Calcium-Mediated Oxidation and Contraction of Mitochondria During Excitotoxicity.
Identifieur interne : 000210 ( Main/Exploration ); précédent : 000209; suivant : 000211Synaptic Activity Protects Neurons Against Calcium-Mediated Oxidation and Contraction of Mitochondria During Excitotoxicity.
Auteurs : Constanze Depp [Allemagne] ; Carlos Bas-Orth [Allemagne] ; Lisa Schroeder [Allemagne] ; Andrea Hellwig [Allemagne] ; Hilmar Bading [Allemagne]Source :
- Antioxidants & redox signaling [ 1557-7716 ] ; 2018.
Descripteurs français
- KwdFr :
- MESH :
- anatomopathologie : Neurones.
- cytologie : Neurones.
- métabolisme : Calcium, Maladies neurodégénératives, Mitochondries, Neurones, Synapses.
- Animaux, Oxydoréduction, Rat Sprague-Dawley, Rats, Stress oxydatif.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Calcium.
- cytology : Neurons.
- metabolism : Mitochondria, Neurodegenerative Diseases, Neurons, Synapses.
- pathology : Neurons.
- Animals, Oxidation-Reduction, Oxidative Stress, Rats, Rats, Sprague-Dawley.
Abstract
AIMS
Excitotoxicity triggered by extrasynaptic N-methyl-d-aspartate-type glutamate receptors has been implicated in many neurodegenerative conditions, including Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, and stroke. Mitochondrial calcium overload leading to mitochondrial dysfunction represents an early event in excitotoxicity. Neurons are rendered resistant to excitotoxicity by previous periods of synaptic activity that activates a nuclear calcium-driven neuroprotective gene program. This process, termed acquired neuroprotection, involves transcriptional repression of the mitochondrial calcium uniporter leading to a reduction in excitotoxcity-associated mitochondrial calcium load. As mitochondrial calcium and the production of reactive oxygen species may be linked, we monitored excitotoxicity-associated changes in the mitochondrial redox status using the ratiometric glutathione redox potential indicator, glutaredoxin 1 (GRX1)-redox-sensitive green fluorescent protein (roGFP)2, targeted to the mitochondrial matrix. Aim of this study was to investigate if suppression of oxidative stress underlies mitoprotection afforded by synaptic activity.
RESULTS
We found that synaptic activity protects primary rat hippocampal neurons against acute excitotoxicity-induced mitochondrial oxidative stress and mitochondrial contraction associated with it. Downregulation of the mitochondrial uniporter by genetic means mimics the protective effect of synaptic activity on mitochondrial redox status. These findings indicate that oxidative stress acts downstream of mitochondrial calcium overload in excitotoxicity. Innovation and Conclusion: We established mito-GRX1-roGFP2 as a reliable and sensitive tool to monitor rapid redox changes in mitochondria during excitotoxicity. Our results highlight the importance of developing means of blocking mitochondrial calcium overload for therapeutic targeting of oxidative stress and mitochondrial dysfunction in neurodegenerative diseases. Antioxid. Redox. Signal. 29, 1109-1124.
DOI: 10.1089/ars.2017.7092
PubMed: 28990420
Affiliations:
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first="Carlos" last="Bas-Orth">Carlos Bas-Orth</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Karlsruhe</region><settlement type="city">Heidelberg</settlement></placeName></affiliation></author><author><name sortKey="Schroeder, Lisa" sort="Schroeder, Lisa" uniqKey="Schroeder L" first="Lisa" last="Schroeder">Lisa Schroeder</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</nlm:affiliation><country 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Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Karlsruhe</region><settlement type="city">Heidelberg</settlement></placeName></affiliation></author><author><name sortKey="Bas Orth, Carlos" sort="Bas Orth, Carlos" uniqKey="Bas Orth C" first="Carlos" last="Bas-Orth">Carlos Bas-Orth</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Karlsruhe</region><settlement type="city">Heidelberg</settlement></placeName></affiliation></author><author><name sortKey="Schroeder, Lisa" sort="Schroeder, Lisa" uniqKey="Schroeder L" first="Lisa" last="Schroeder">Lisa Schroeder</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Karlsruhe</region><settlement type="city">Heidelberg</settlement></placeName></affiliation></author><author><name sortKey="Hellwig, Andrea" sort="Hellwig, Andrea" uniqKey="Hellwig A" first="Andrea" last="Hellwig">Andrea Hellwig</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Karlsruhe</region><settlement type="city">Heidelberg</settlement></placeName></affiliation></author><author><name sortKey="Bading, Hilmar" sort="Bading, Hilmar" uniqKey="Bading H" first="Hilmar" last="Bading">Hilmar Bading</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Karlsruhe</region><settlement type="city">Heidelberg</settlement></placeName></affiliation></author></analytic><series><title level="j">Antioxidants & redox signaling</title><idno type="eISSN">1557-7716</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Calcium (metabolism)</term><term>Mitochondria (metabolism)</term><term>Neurodegenerative Diseases (metabolism)</term><term>Neurons (cytology)</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Oxidation-Reduction (MeSH)</term><term>Oxidative Stress (MeSH)</term><term>Rats (MeSH)</term><term>Rats, Sprague-Dawley (MeSH)</term><term>Synapses (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Calcium (métabolisme)</term><term>Maladies neurodégénératives (métabolisme)</term><term>Mitochondries (métabolisme)</term><term>Neurones (anatomopathologie)</term><term>Neurones (cytologie)</term><term>Neurones (métabolisme)</term><term>Oxydoréduction (MeSH)</term><term>Rat Sprague-Dawley (MeSH)</term><term>Rats (MeSH)</term><term>Stress oxydatif (MeSH)</term><term>Synapses (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcium</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Neurones</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Neurones</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mitochondria</term><term>Neurodegenerative Diseases</term><term>Neurons</term><term>Synapses</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Calcium</term><term>Maladies neurodégénératives</term><term>Mitochondries</term><term>Neurones</term><term>Synapses</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Oxidation-Reduction</term><term>Oxidative Stress</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Oxydoréduction</term><term>Rat Sprague-Dawley</term><term>Rats</term><term>Stress oxydatif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>AIMS</b></p><p>Excitotoxicity triggered by extrasynaptic N-methyl-d-aspartate-type glutamate receptors has been implicated in many neurodegenerative conditions, including Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, and stroke. Mitochondrial calcium overload leading to mitochondrial dysfunction represents an early event in excitotoxicity. Neurons are rendered resistant to excitotoxicity by previous periods of synaptic activity that activates a nuclear calcium-driven neuroprotective gene program. This process, termed acquired neuroprotection, involves transcriptional repression of the mitochondrial calcium uniporter leading to a reduction in excitotoxcity-associated mitochondrial calcium load. As mitochondrial calcium and the production of reactive oxygen species may be linked, we monitored excitotoxicity-associated changes in the mitochondrial redox status using the ratiometric glutathione redox potential indicator, glutaredoxin 1 (GRX1)-redox-sensitive green fluorescent protein (roGFP)2, targeted to the mitochondrial matrix. Aim of this study was to investigate if suppression of oxidative stress underlies mitoprotection afforded by synaptic activity.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>We found that synaptic activity protects primary rat hippocampal neurons against acute excitotoxicity-induced mitochondrial oxidative stress and mitochondrial contraction associated with it. Downregulation of the mitochondrial uniporter by genetic means mimics the protective effect of synaptic activity on mitochondrial redox status. These findings indicate that oxidative stress acts downstream of mitochondrial calcium overload in excitotoxicity. Innovation and Conclusion: We established mito-GRX1-roGFP2 as a reliable and sensitive tool to monitor rapid redox changes in mitochondria during excitotoxicity. Our results highlight the importance of developing means of blocking mitochondrial calcium overload for therapeutic targeting of oxidative stress and mitochondrial dysfunction in neurodegenerative diseases. Antioxid. Redox. Signal. 29, 1109-1124.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28990420</PMID><DateCompleted><Year>2019</Year><Month>09</Month><Day>30</Day></DateCompleted><DateRevised><Year>2019</Year><Month>09</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1557-7716</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><Issue>12</Issue><PubDate><Year>2018</Year><Month>10</Month><Day>20</Day></PubDate></JournalIssue><Title>Antioxidants & redox signaling</Title><ISOAbbreviation>Antioxid Redox Signal</ISOAbbreviation></Journal><ArticleTitle>Synaptic Activity Protects Neurons Against Calcium-Mediated Oxidation and Contraction of Mitochondria During Excitotoxicity.</ArticleTitle><Pagination><MedlinePgn>1109-1124</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1089/ars.2017.7092</ELocationID><Abstract><AbstractText Label="AIMS">Excitotoxicity triggered by extrasynaptic N-methyl-d-aspartate-type glutamate receptors has been implicated in many neurodegenerative conditions, including Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, and stroke. Mitochondrial calcium overload leading to mitochondrial dysfunction represents an early event in excitotoxicity. Neurons are rendered resistant to excitotoxicity by previous periods of synaptic activity that activates a nuclear calcium-driven neuroprotective gene program. This process, termed acquired neuroprotection, involves transcriptional repression of the mitochondrial calcium uniporter leading to a reduction in excitotoxcity-associated mitochondrial calcium load. As mitochondrial calcium and the production of reactive oxygen species may be linked, we monitored excitotoxicity-associated changes in the mitochondrial redox status using the ratiometric glutathione redox potential indicator, glutaredoxin 1 (GRX1)-redox-sensitive green fluorescent protein (roGFP)2, targeted to the mitochondrial matrix. Aim of this study was to investigate if suppression of oxidative stress underlies mitoprotection afforded by synaptic activity.</AbstractText><AbstractText Label="RESULTS">We found that synaptic activity protects primary rat hippocampal neurons against acute excitotoxicity-induced mitochondrial oxidative stress and mitochondrial contraction associated with it. Downregulation of the mitochondrial uniporter by genetic means mimics the protective effect of synaptic activity on mitochondrial redox status. These findings indicate that oxidative stress acts downstream of mitochondrial calcium overload in excitotoxicity. Innovation and Conclusion: We established mito-GRX1-roGFP2 as a reliable and sensitive tool to monitor rapid redox changes in mitochondria during excitotoxicity. Our results highlight the importance of developing means of blocking mitochondrial calcium overload for therapeutic targeting of oxidative stress and mitochondrial dysfunction in neurodegenerative diseases. Antioxid. Redox. Signal. 29, 1109-1124.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Depp</LastName><ForeName>Constanze</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bas-Orth</LastName><ForeName>Carlos</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schroeder</LastName><ForeName>Lisa</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hellwig</LastName><ForeName>Andrea</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bading</LastName><ForeName>Hilmar</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Neurobiology, Interdisciplinary Center for Neurosciences, Heidelberg University , Heidelberg, Germany .</Affiliation></AffiliationInfo></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>2017</Year><Month>11</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Antioxid Redox Signal</MedlineTA><NlmUniqueID>100888899</NlmUniqueID><ISSNLinking>1523-0864</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019636" MajorTopicYN="N">Neurodegenerative Diseases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013569" MajorTopicYN="N">Synapses</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">acquired neuroprotection</Keyword><Keyword MajorTopicYN="Y">calcium signaling</Keyword><Keyword MajorTopicYN="Y">excitotoxicity</Keyword><Keyword MajorTopicYN="Y">gene regulation</Keyword><Keyword MajorTopicYN="Y">mitochondria</Keyword><Keyword MajorTopicYN="Y">oxidation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>10</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>10</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>10</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28990420</ArticleId><ArticleId IdType="doi">10.1089/ars.2017.7092</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country><region><li>Bade-Wurtemberg</li><li>District de Karlsruhe</li></region><settlement><li>Heidelberg</li></settlement></list><tree><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Depp, Constanze" sort="Depp, Constanze" uniqKey="Depp C" first="Constanze" last="Depp">Constanze Depp</name></region><name sortKey="Bading, Hilmar" sort="Bading, Hilmar" uniqKey="Bading H" first="Hilmar" last="Bading">Hilmar Bading</name><name sortKey="Bas Orth, Carlos" sort="Bas Orth, Carlos" uniqKey="Bas Orth C" first="Carlos" last="Bas-Orth">Carlos Bas-Orth</name><name sortKey="Hellwig, Andrea" sort="Hellwig, Andrea" uniqKey="Hellwig A" first="Andrea" last="Hellwig">Andrea Hellwig</name><name sortKey="Schroeder, Lisa" sort="Schroeder, Lisa" uniqKey="Schroeder L" first="Lisa" last="Schroeder">Lisa Schroeder</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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