Electromyographic characterization in an animal model of dystonia.
Identifieur interne : 002238 ( PubMed/Curation ); précédent : 002237; suivant : 002239Electromyographic characterization in an animal model of dystonia.
Auteurs : Kunal Chaniary [États-Unis] ; Mark Baron ; Ann Rice ; Paul Wetzel ; Steven ShapiroSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Animals, Disease Models, Animal, Dystonia (chemically induced), Dystonia (physiopathology), Electromyography, Fourier Analysis, Kernicterus (physiopathology), Motor Neurons (physiology), Muscle Contraction (physiology), Muscle, Skeletal (innervation), Rats, Rats, Gunn, Signal Processing, Computer-Assisted, Sulfadimethoxine.
- MESH :
- chemical : Sulfadimethoxine.
- chemically induced : Dystonia.
- innervation : Muscle, Skeletal.
- physiology : Motor Neurons, Muscle Contraction.
- physiopathology : Dystonia, Kernicterus.
- Animals, Disease Models, Animal, Electromyography, Fourier Analysis, Rats, Rats, Gunn, Signal Processing, Computer-Assisted.
Abstract
Kernicterus is known to produce damage to the auditory system and the basal ganglia in humans. Although the Gunn rat model of kernicterus has been extensively used to characterize the auditory features, this model has not been similarly utilized to systematically investigate the movement disorder. In the present study, spontaneously jaundiced (jj) 16 day old Gunn rat pups were treated with sulfadimethoxine to exacerbate bilirubin toxicity and compared to saline treated jjs and non-jaundiced (Nj) littermates. Electromyographic (EMG) activity was recorded from antagonistic hip muscles in dystonic and in normal appearing rats. Raw EMG signals were decomposed using the Discrete Wavelet Transform based multi-resolution analysis and signal coefficients corresponding to the dominant EMG frequency band were chosen. Gunn rats exposed to sulfadimethoxine developed a stable clinical state characterized by prolonged abnormal axial and appendicular postures. Coherence plots of the separated signals coefficients revealed 4-7 Hz co-activation in antagonistic muscles that was significantly more prominent in jj sulfa treated dystonic compared to normal rats. The EMG findings support the presence of dystonia in sulfadimethoxine exposed jj Gunn rats and suggest that these animals can serve as a valuable model for experimental investigations of dystonia.
DOI: 10.1002/mds.22040
PubMed: 18442136
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Although the Gunn rat model of kernicterus has been extensively used to characterize the auditory features, this model has not been similarly utilized to systematically investigate the movement disorder. In the present study, spontaneously jaundiced (jj) 16 day old Gunn rat pups were treated with sulfadimethoxine to exacerbate bilirubin toxicity and compared to saline treated jjs and non-jaundiced (Nj) littermates. Electromyographic (EMG) activity was recorded from antagonistic hip muscles in dystonic and in normal appearing rats. Raw EMG signals were decomposed using the Discrete Wavelet Transform based multi-resolution analysis and signal coefficients corresponding to the dominant EMG frequency band were chosen. Gunn rats exposed to sulfadimethoxine developed a stable clinical state characterized by prolonged abnormal axial and appendicular postures. Coherence plots of the separated signals coefficients revealed 4-7 Hz co-activation in antagonistic muscles that was significantly more prominent in jj sulfa treated dystonic compared to normal rats. The EMG findings support the presence of dystonia in sulfadimethoxine exposed jj Gunn rats and suggest that these animals can serve as a valuable model for experimental investigations of dystonia.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">18442136</PMID><DateCreated><Year>2008</Year><Month>07</Month><Day>10</Day></DateCreated><DateCompleted><Year>2008</Year><Month>10</Month><Day>20</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>8</Issue><PubDate><Year>2008</Year><Month>Jun</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Electromyographic characterization in an animal model of dystonia.</ArticleTitle><Pagination><MedlinePgn>1122-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22040</ELocationID><Abstract><AbstractText>Kernicterus is known to produce damage to the auditory system and the basal ganglia in humans. Although the Gunn rat model of kernicterus has been extensively used to characterize the auditory features, this model has not been similarly utilized to systematically investigate the movement disorder. In the present study, spontaneously jaundiced (jj) 16 day old Gunn rat pups were treated with sulfadimethoxine to exacerbate bilirubin toxicity and compared to saline treated jjs and non-jaundiced (Nj) littermates. Electromyographic (EMG) activity was recorded from antagonistic hip muscles in dystonic and in normal appearing rats. Raw EMG signals were decomposed using the Discrete Wavelet Transform based multi-resolution analysis and signal coefficients corresponding to the dominant EMG frequency band were chosen. Gunn rats exposed to sulfadimethoxine developed a stable clinical state characterized by prolonged abnormal axial and appendicular postures. Coherence plots of the separated signals coefficients revealed 4-7 Hz co-activation in antagonistic muscles that was significantly more prominent in jj sulfa treated dystonic compared to normal rats. The EMG findings support the presence of dystonia in sulfadimethoxine exposed jj Gunn rats and suggest that these animals can serve as a valuable model for experimental investigations of dystonia.</AbstractText><CopyrightInformation>(c) 2008 Movement Disorder Society</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chaniary</LastName><ForeName>Kunal</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Biomedical Engineering, Virginia Commonwealth University, Richmond, Virginia, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baron</LastName><ForeName>Mark</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Rice</LastName><ForeName>Ann</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Wetzel</LastName><ForeName>Paul</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Shapiro</LastName><ForeName>Steven</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01NS47151</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>30CPC5LDEX</RegistryNumber><NameOfSubstance UI="D013412">Sulfadimethoxine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D004195">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004421">Dystonia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000139">chemically induced</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D004576">Electromyography</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005583">Fourier Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007647">Kernicterus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009046">Motor Neurons</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009119">Muscle Contraction</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018482">Muscle, Skeletal</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000294">innervation</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011911">Rats, Gunn</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D012815">Signal Processing, Computer-Assisted</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013412">Sulfadimethoxine</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>4</Month><Day>30</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>10</Month><Day>22</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>4</Month><Day>30</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.22040</ArticleId><ArticleId IdType="pubmed">18442136</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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