Elevated Mitochondrial Bioenergetics and Axonal Arborization Size Are Key Contributors to the Vulnerability of Dopamine Neurons.
Identifieur interne : 000412 ( PubMed/Curation ); précédent : 000411; suivant : 000413Elevated Mitochondrial Bioenergetics and Axonal Arborization Size Are Key Contributors to the Vulnerability of Dopamine Neurons.
Auteurs : Consiglia Pacelli [Canada] ; Nicolas Giguère [Canada] ; Marie-Josée Bourque [Canada] ; Martin Lévesque [Canada] ; Ruth S. Slack [Canada] ; Louis-Éric Trudeau [Canada]Source :
- Current biology : CB [ 1879-0445 ] ; 2015.
English descriptors
- KwdEn :
- 1-Methyl-4-phenylpyridinium (pharmacology), Animals, Axons (physiology), Dopaminergic Neurons (physiology), Energy Metabolism, Hydrogen Peroxide (pharmacology), Mice, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria (metabolism), Neuronal Plasticity, Neurotoxins (pharmacology), Oxidative Phosphorylation, Parkinson Disease (metabolism), Pars Compacta (physiology), Rotenone (pharmacology), Ventral Tegmental Area (physiology).
- MESH :
- chemical , pharmacology : 1-Methyl-4-phenylpyridinium, Hydrogen Peroxide, Neurotoxins, Rotenone.
- metabolism : Mitochondria, Parkinson Disease.
- physiology : Axons, Dopaminergic Neurons, Pars Compacta, Ventral Tegmental Area.
- Animals, Energy Metabolism, Mice, Mice, Inbred C57BL, Mice, Transgenic, Neuronal Plasticity, Oxidative Phosphorylation.
Abstract
Although the mechanisms underlying the loss of neurons in Parkinson's disease are not well understood, impaired mitochondrial function and pathological protein aggregation are suspected as playing a major role. Why DA (dopamine) neurons and a select small subset of brain nuclei are particularly vulnerable to such ubiquitous cellular dysfunctions is presently one of the key unanswered questions in Parkinson's disease research. One intriguing hypothesis is that their heightened vulnerability is a consequence of their elevated bioenergetic requirements. Here, we show for the first time that vulnerable nigral DA neurons differ from less vulnerable DA neurons such as those of the VTA (ventral tegmental area) by having a higher basal rate of mitochondrial OXPHOS (oxidative phosphorylation), a smaller reserve capacity, a higher density of axonal mitochondria, an elevated level of basal oxidative stress, and a considerably more complex axonal arborization. Furthermore, we demonstrate that reducing axonal arborization by acting on axon guidance pathways with Semaphorin 7A reduces in parallel the basal rate of mitochondrial OXPHOS and the vulnerability of nigral DA neurons to the neurotoxic agents MPP(+) (1-methyl-4-phenylpyridinium) and rotenone. Blocking L-type calcium channels with isradipine was protective against MPP(+) but not rotenone. Our data provide the most direct demonstration to date in favor of the hypothesis that the heightened vulnerability of nigral DA neurons in Parkinson's disease is directly due to their particular bioenergetic and morphological characteristics.
DOI: 10.1016/j.cub.2015.07.050
PubMed: 26320949
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Slack</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5</wicri:regionArea></affiliation></author><author><name sortKey="Trudeau, Louis Eric" sort="Trudeau, Louis Eric" uniqKey="Trudeau L" first="Louis-Éric" last="Trudeau">Louis-Éric Trudeau</name><affiliation wicri:level="1"><nlm:affiliation>Departments of Pharmacology and Neurosciences, Central Nervous System Research Group (GRSNC), Faculty of Medicine, Université de Montréal, Montréal, QC H4T 1J4, Canada. Electronic address: louis-eric.trudeau@umontreal.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Departments of Pharmacology and Neurosciences, Central Nervous System Research Group (GRSNC), Faculty of Medicine, Université de Montréal, Montréal, QC H4T 1J4</wicri:regionArea></affiliation></author></analytic><series><title level="j">Current biology : CB</title><idno type="eISSN">1879-0445</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenylpyridinium (pharmacology)</term><term>Animals</term><term>Axons (physiology)</term><term>Dopaminergic Neurons (physiology)</term><term>Energy Metabolism</term><term>Hydrogen Peroxide (pharmacology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Mitochondria (metabolism)</term><term>Neuronal Plasticity</term><term>Neurotoxins (pharmacology)</term><term>Oxidative Phosphorylation</term><term>Parkinson Disease (metabolism)</term><term>Pars Compacta (physiology)</term><term>Rotenone (pharmacology)</term><term>Ventral Tegmental Area (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>1-Methyl-4-phenylpyridinium</term><term>Hydrogen Peroxide</term><term>Neurotoxins</term><term>Rotenone</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mitochondria</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Axons</term><term>Dopaminergic Neurons</term><term>Pars Compacta</term><term>Ventral Tegmental Area</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Energy Metabolism</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Neuronal Plasticity</term><term>Oxidative Phosphorylation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although the mechanisms underlying the loss of neurons in Parkinson's disease are not well understood, impaired mitochondrial function and pathological protein aggregation are suspected as playing a major role. Why DA (dopamine) neurons and a select small subset of brain nuclei are particularly vulnerable to such ubiquitous cellular dysfunctions is presently one of the key unanswered questions in Parkinson's disease research. One intriguing hypothesis is that their heightened vulnerability is a consequence of their elevated bioenergetic requirements. Here, we show for the first time that vulnerable nigral DA neurons differ from less vulnerable DA neurons such as those of the VTA (ventral tegmental area) by having a higher basal rate of mitochondrial OXPHOS (oxidative phosphorylation), a smaller reserve capacity, a higher density of axonal mitochondria, an elevated level of basal oxidative stress, and a considerably more complex axonal arborization. Furthermore, we demonstrate that reducing axonal arborization by acting on axon guidance pathways with Semaphorin 7A reduces in parallel the basal rate of mitochondrial OXPHOS and the vulnerability of nigral DA neurons to the neurotoxic agents MPP(+) (1-methyl-4-phenylpyridinium) and rotenone. Blocking L-type calcium channels with isradipine was protective against MPP(+) but not rotenone. Our data provide the most direct demonstration to date in favor of the hypothesis that the heightened vulnerability of nigral DA neurons in Parkinson's disease is directly due to their particular bioenergetic and morphological characteristics.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26320949</PMID><DateCreated><Year>2015</Year><Month>09</Month><Day>23</Day></DateCreated><DateCompleted><Year>2016</Year><Month>06</Month><Day>17</Day></DateCompleted><DateRevised><Year>2015</Year><Month>09</Month><Day>23</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0445</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>18</Issue><PubDate><Year>2015</Year><Month>Sep</Month><Day>21</Day></PubDate></JournalIssue><Title>Current biology : CB</Title><ISOAbbreviation>Curr. Biol.</ISOAbbreviation></Journal><ArticleTitle>Elevated Mitochondrial Bioenergetics and Axonal Arborization Size Are Key Contributors to the Vulnerability of Dopamine Neurons.</ArticleTitle><Pagination><MedlinePgn>2349-60</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cub.2015.07.050</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0960-9822(15)00884-2</ELocationID><Abstract><AbstractText>Although the mechanisms underlying the loss of neurons in Parkinson's disease are not well understood, impaired mitochondrial function and pathological protein aggregation are suspected as playing a major role. Why DA (dopamine) neurons and a select small subset of brain nuclei are particularly vulnerable to such ubiquitous cellular dysfunctions is presently one of the key unanswered questions in Parkinson's disease research. One intriguing hypothesis is that their heightened vulnerability is a consequence of their elevated bioenergetic requirements. Here, we show for the first time that vulnerable nigral DA neurons differ from less vulnerable DA neurons such as those of the VTA (ventral tegmental area) by having a higher basal rate of mitochondrial OXPHOS (oxidative phosphorylation), a smaller reserve capacity, a higher density of axonal mitochondria, an elevated level of basal oxidative stress, and a considerably more complex axonal arborization. Furthermore, we demonstrate that reducing axonal arborization by acting on axon guidance pathways with Semaphorin 7A reduces in parallel the basal rate of mitochondrial OXPHOS and the vulnerability of nigral DA neurons to the neurotoxic agents MPP(+) (1-methyl-4-phenylpyridinium) and rotenone. Blocking L-type calcium channels with isradipine was protective against MPP(+) but not rotenone. Our data provide the most direct demonstration to date in favor of the hypothesis that the heightened vulnerability of nigral DA neurons in Parkinson's disease is directly due to their particular bioenergetic and morphological characteristics.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pacelli</LastName><ForeName>Consiglia</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Departments of Pharmacology and Neurosciences, Central Nervous System Research Group (GRSNC), Faculty of Medicine, Université de Montréal, Montréal, QC H4T 1J4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Giguère</LastName><ForeName>Nicolas</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Departments of Pharmacology and Neurosciences, Central Nervous System Research Group (GRSNC), Faculty of Medicine, Université de Montréal, Montréal, QC H4T 1J4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bourque</LastName><ForeName>Marie-Josée</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Departments of Pharmacology and Neurosciences, Central Nervous System Research Group (GRSNC), Faculty of Medicine, Université de Montréal, Montréal, QC H4T 1J4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lévesque</LastName><ForeName>Martin</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Psychiatry and Neurosciences, Centre de Recherche de l'Institut Universitaire en Santé Mentale de Québec, Faculté de Médecine, Université Laval, Québec, QC G1J 2G3, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Slack</LastName><ForeName>Ruth S</ForeName><Initials>RS</Initials><AffiliationInfo><Affiliation>Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Trudeau</LastName><ForeName>Louis-Éric</ForeName><Initials>LÉ</Initials><AffiliationInfo><Affiliation>Departments of Pharmacology and Neurosciences, Central Nervous System Research Group (GRSNC), Faculty of Medicine, Université de Montréal, Montréal, QC H4T 1J4, Canada. Electronic address: louis-eric.trudeau@umontreal.ca.</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>2015</Year><Month>08</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Curr Biol</MedlineTA><NlmUniqueID>9107782</NlmUniqueID><ISSNLinking>0960-9822</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009498">Neurotoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>03L9OT429T</RegistryNumber><NameOfSubstance UI="D012402">Rotenone</NameOfSubstance></Chemical><Chemical><RegistryNumber>BBX060AN9V</RegistryNumber><NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>R865A5OY8J</RegistryNumber><NameOfSubstance UI="D015655">1-Methyl-4-phenylpyridinium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Curr Biol. 2015 Sep 21;25(18):R797-800</RefSource><PMID Version="1">26394101</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D015655" MajorTopicYN="N">1-Methyl-4-phenylpyridinium</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001369" MajorTopicYN="N">Axons</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059290" MajorTopicYN="N">Dopaminergic Neurons</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004734" MajorTopicYN="Y">Energy Metabolism</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009473" MajorTopicYN="Y">Neuronal Plasticity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009498" MajorTopicYN="N">Neurotoxins</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010085" MajorTopicYN="N">Oxidative Phosphorylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D065842" MajorTopicYN="N">Pars Compacta</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012402" MajorTopicYN="N">Rotenone</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017557" MajorTopicYN="N">Ventral Tegmental Area</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>02</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>06</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>07</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>9</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>9</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>6</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26320949</ArticleId><ArticleId IdType="pii">S0960-9822(15)00884-2</ArticleId><ArticleId IdType="doi">10.1016/j.cub.2015.07.050</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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