Deletion of the vesicular acetylcholine transporter from pedunculopontine/laterodorsal tegmental neurons modifies gait.
Identifieur interne : 000084 ( PubMed/Checkpoint ); précédent : 000083; suivant : 000085Deletion of the vesicular acetylcholine transporter from pedunculopontine/laterodorsal tegmental neurons modifies gait.
Auteurs : Helena Janickova [Canada] ; Kaie Rosborough [Canada] ; Mohammed Al-Onaizi [Canada] ; Ornela Kljakic [Canada] ; Monica S. Guzman [Canada] ; Robert Gros [Canada] ; Marco A M. Prado [Canada] ; Vania F. Prado [Canada]Source :
- Journal of neurochemistry [ 1471-4159 ] ; 2017.
Abstract
Postural instability and gait disturbances, common disabilities in the elderly and frequently present in Parkinson's disease (PD), have been suggested to be related to dysfunctional cholinergic signaling in the brainstem. We investigated how long-term loss of cholinergic signaling from mesopontine nuclei influence motor behaviors. We selectively eliminated the vesicular acetylcholine transporter (VAChT) in pedunculopontine and laterodorsal tegmental nuclei cholinergic neurons to generate mice with selective mesopontine cholinergic deficiency (VAChT(E)(n1-Cre-flox/flox) ). VAChT(E)(n1-Cre-flox/flox) mice did not show any gross health or neuromuscular abnormality on metabolic cages, wire-hang and grip-force tests. Young VAChT(E)(n1-Cre-flox/flox) mice (2-5 months-old) presented motor learning/coordination deficits on the rotarod; moved slower, and had smaller steps on the catwalk, but showed no difference in locomotor activity on the open field. Old VAChT(E)(n1-Creflox/flox) mice (13-16 months-old) showed more pronounced motor learning/balance deficits on the rotarod, and more pronounced balance deficits on the catwalk. Furthermore, old mutants moved faster than controls, but with similar step length. Additionally, old VAChT-deficient mice were hyperactive. These results suggest that dysfunction of cholinergic neurons from mesopontine nuclei, which is commonly seen in PD, has causal roles in motor functions. Prevention of mesopontine cholinergic failure may help to prevent/improve postural instability and falls in PD patients. Read the Editorial Highlight for this article on page 688.
DOI: 10.1111/jnc.13910
PubMed: 27889925
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Guzman</name><affiliation wicri:level="1"><nlm:affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Gros, Robert" sort="Gros, Robert" uniqKey="Gros R" first="Robert" last="Gros">Robert Gros</name><affiliation wicri:level="1"><nlm:affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Prado, Marco A M" sort="Prado, Marco A M" uniqKey="Prado M" first="Marco A M" last="Prado">Marco A M. Prado</name><affiliation wicri:level="1"><nlm:affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Prado, Vania F" sort="Prado, Vania F" uniqKey="Prado V" first="Vania F" last="Prado">Vania F. Prado</name><affiliation wicri:level="1"><nlm:affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of neurochemistry</title><idno type="eISSN">1471-4159</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Postural instability and gait disturbances, common disabilities in the elderly and frequently present in Parkinson's disease (PD), have been suggested to be related to dysfunctional cholinergic signaling in the brainstem. We investigated how long-term loss of cholinergic signaling from mesopontine nuclei influence motor behaviors. We selectively eliminated the vesicular acetylcholine transporter (VAChT) in pedunculopontine and laterodorsal tegmental nuclei cholinergic neurons to generate mice with selective mesopontine cholinergic deficiency (VAChT(E)(n1-Cre-flox/flox) ). VAChT(E)(n1-Cre-flox/flox) mice did not show any gross health or neuromuscular abnormality on metabolic cages, wire-hang and grip-force tests. Young VAChT(E)(n1-Cre-flox/flox) mice (2-5 months-old) presented motor learning/coordination deficits on the rotarod; moved slower, and had smaller steps on the catwalk, but showed no difference in locomotor activity on the open field. Old VAChT(E)(n1-Creflox/flox) mice (13-16 months-old) showed more pronounced motor learning/balance deficits on the rotarod, and more pronounced balance deficits on the catwalk. Furthermore, old mutants moved faster than controls, but with similar step length. Additionally, old VAChT-deficient mice were hyperactive. These results suggest that dysfunction of cholinergic neurons from mesopontine nuclei, which is commonly seen in PD, has causal roles in motor functions. Prevention of mesopontine cholinergic failure may help to prevent/improve postural instability and falls in PD patients. Read the Editorial Highlight for this article on page 688.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">27889925</PMID><DateCreated><Year>2016</Year><Month>11</Month><Day>27</Day></DateCreated><DateRevised><Year>2017</Year><Month>02</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1471-4159</ISSN><JournalIssue CitedMedium="Internet"><Volume>140</Volume><Issue>5</Issue><PubDate><Year>2017</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Journal of neurochemistry</Title><ISOAbbreviation>J. Neurochem.</ISOAbbreviation></Journal><ArticleTitle>Deletion of the vesicular acetylcholine transporter from pedunculopontine/laterodorsal tegmental neurons modifies gait.</ArticleTitle><Pagination><MedlinePgn>787-798</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/jnc.13910</ELocationID><Abstract><AbstractText>Postural instability and gait disturbances, common disabilities in the elderly and frequently present in Parkinson's disease (PD), have been suggested to be related to dysfunctional cholinergic signaling in the brainstem. We investigated how long-term loss of cholinergic signaling from mesopontine nuclei influence motor behaviors. We selectively eliminated the vesicular acetylcholine transporter (VAChT) in pedunculopontine and laterodorsal tegmental nuclei cholinergic neurons to generate mice with selective mesopontine cholinergic deficiency (VAChT(E)(n1-Cre-flox/flox) ). VAChT(E)(n1-Cre-flox/flox) mice did not show any gross health or neuromuscular abnormality on metabolic cages, wire-hang and grip-force tests. Young VAChT(E)(n1-Cre-flox/flox) mice (2-5 months-old) presented motor learning/coordination deficits on the rotarod; moved slower, and had smaller steps on the catwalk, but showed no difference in locomotor activity on the open field. Old VAChT(E)(n1-Creflox/flox) mice (13-16 months-old) showed more pronounced motor learning/balance deficits on the rotarod, and more pronounced balance deficits on the catwalk. Furthermore, old mutants moved faster than controls, but with similar step length. Additionally, old VAChT-deficient mice were hyperactive. These results suggest that dysfunction of cholinergic neurons from mesopontine nuclei, which is commonly seen in PD, has causal roles in motor functions. Prevention of mesopontine cholinergic failure may help to prevent/improve postural instability and falls in PD patients. Read the Editorial Highlight for this article on page 688.</AbstractText><CopyrightInformation>© 2016 International Society for Neurochemistry.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Janickova</LastName><ForeName>Helena</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rosborough</LastName><ForeName>Kaie</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anatomy and Cell Biology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Al-Onaizi</LastName><ForeName>Mohammed</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anatomy and Cell Biology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kljakic</LastName><ForeName>Ornela</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anatomy and Cell Biology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guzman</LastName><ForeName>Monica S</ForeName><Initials>MS</Initials><AffiliationInfo><Affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anatomy and Cell Biology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gros</LastName><ForeName>Robert</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Physiology and Pharmacology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Prado</LastName><ForeName>Marco A M</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anatomy and Cell Biology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Physiology and Pharmacology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Prado</LastName><ForeName>Vania F</ForeName><Initials>VF</Initials><AffiliationInfo><Affiliation>Robarts Research Institute, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anatomy and Cell Biology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Physiology and Pharmacology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>01</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neurochem</MedlineTA><NlmUniqueID>2985190R</NlmUniqueID><ISSNLinking>0022-3042</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">acetylcholine</Keyword><Keyword MajorTopicYN="N">balance</Keyword><Keyword MajorTopicYN="N">gait</Keyword><Keyword MajorTopicYN="N">motor disease</Keyword><Keyword MajorTopicYN="N">pedunculopontine</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>09</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>11</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>11</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>11</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>11</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>11</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27889925</ArticleId><ArticleId IdType="doi">10.1111/jnc.13910</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Janickova, Helena" sort="Janickova, Helena" uniqKey="Janickova H" first="Helena" last="Janickova">Helena Janickova</name></noRegion><name sortKey="Al Onaizi, Mohammed" sort="Al Onaizi, Mohammed" uniqKey="Al Onaizi M" first="Mohammed" last="Al-Onaizi">Mohammed Al-Onaizi</name><name sortKey="Gros, Robert" sort="Gros, Robert" uniqKey="Gros R" first="Robert" last="Gros">Robert Gros</name><name sortKey="Guzman, Monica S" sort="Guzman, Monica S" uniqKey="Guzman M" first="Monica S" last="Guzman">Monica S. Guzman</name><name sortKey="Kljakic, Ornela" sort="Kljakic, Ornela" uniqKey="Kljakic O" first="Ornela" last="Kljakic">Ornela Kljakic</name><name sortKey="Prado, Marco A M" sort="Prado, Marco A M" uniqKey="Prado M" first="Marco A M" last="Prado">Marco A M. Prado</name><name sortKey="Prado, Vania F" sort="Prado, Vania F" uniqKey="Prado V" first="Vania F" last="Prado">Vania F. Prado</name><name sortKey="Rosborough, Kaie" sort="Rosborough, Kaie" uniqKey="Rosborough K" first="Kaie" last="Rosborough">Kaie Rosborough</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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