Chronic but not acute dopaminergic transmission interruption promotes a progressive increase in cortical beta frequency synchronization: relationships to vigilance state and akinesia.
Identifieur interne : 000B37 ( PubMed/Checkpoint ); précédent : 000B36; suivant : 000B38Chronic but not acute dopaminergic transmission interruption promotes a progressive increase in cortical beta frequency synchronization: relationships to vigilance state and akinesia.
Auteurs : Bertrand Degos [France] ; Jean-Michel Deniau ; Mario Chavez ; Nicolas MauriceSource :
- Cerebral cortex (New York, N.Y. : 1991) [ 1460-2199 ] ; 2009.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Dopamine.
- physiopathology : Basal Ganglia, Cerebral Cortex, Parkinson Disease.
- Animals, Arousal, Biological Clocks, Cortical Synchronization, Disease Models, Animal, Humans, Male, Rats, Rats, Sprague-Dawley, Synaptic Transmission.
Abstract
Dopaminergic (DA) denervation results in the appearance of an excessive cortical beta frequency synchronization in parkinsonian patients and animal models of the disease. The present study analyzed electrocorticogram signals in awake rats to further characterize this excessive synchronization in terms of time course, relation to motor activity and state of vigilance. Using substantia nigra pars compacta lesions and both acute and chronic pharmacological interruptions of DA transmission, the present data demonstrated that the appearance of excessive beta synchronization requires a prolonged interruption in DA transmission and builds up progressively. This synchronization was vigilance-state dependent and observed solely during awake-like activity. Furthermore, these data demonstrated for the first time that the appearance of akinesia preceded the excessive cortical beta synchronization. In addition, this synchronization was stronger in the motor than in the somato-sensory cortex and in unilaterally compared with bilaterally lesioned animals. Finally, excessive beta synchronization was accompanied by an increased coherence between motor and somato-sensory cortical activities. These data suggest that excessive beta synchronization is associated with plastic processes whose time course is delayed with respect to the akinesia. Moreover, the expression of this phenomenon, which likely reflects functional changes in the cortico-basal ganglia circuits, requires a specific brain state.
DOI: 10.1093/cercor/bhn199
PubMed: 18996909
Affiliations:
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xml:lang="en">Dopaminergic (DA) denervation results in the appearance of an excessive cortical beta frequency synchronization in parkinsonian patients and animal models of the disease. The present study analyzed electrocorticogram signals in awake rats to further characterize this excessive synchronization in terms of time course, relation to motor activity and state of vigilance. Using substantia nigra pars compacta lesions and both acute and chronic pharmacological interruptions of DA transmission, the present data demonstrated that the appearance of excessive beta synchronization requires a prolonged interruption in DA transmission and builds up progressively. This synchronization was vigilance-state dependent and observed solely during awake-like activity. Furthermore, these data demonstrated for the first time that the appearance of akinesia preceded the excessive cortical beta synchronization. In addition, this synchronization was stronger in the motor than in the somato-sensory cortex and in unilaterally compared with bilaterally lesioned animals. Finally, excessive beta synchronization was accompanied by an increased coherence between motor and somato-sensory cortical activities. These data suggest that excessive beta synchronization is associated with plastic processes whose time course is delayed with respect to the akinesia. Moreover, the expression of this phenomenon, which likely reflects functional changes in the cortico-basal ganglia circuits, requires a specific brain state.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18996909</PMID><DateCreated><Year>2009</Year><Month>06</Month><Day>10</Day></DateCreated><DateCompleted><Year>2009</Year><Month>08</Month><Day>26</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2199</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>7</Issue><PubDate><Year>2009</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Cerebral cortex (New York, N.Y. : 1991)</Title><ISOAbbreviation>Cereb. Cortex</ISOAbbreviation></Journal><ArticleTitle>Chronic but not acute dopaminergic transmission interruption promotes a progressive increase in cortical beta frequency synchronization: relationships to vigilance state and akinesia.</ArticleTitle><Pagination><MedlinePgn>1616-30</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/cercor/bhn199</ELocationID><Abstract><AbstractText>Dopaminergic (DA) denervation results in the appearance of an excessive cortical beta frequency synchronization in parkinsonian patients and animal models of the disease. The present study analyzed electrocorticogram signals in awake rats to further characterize this excessive synchronization in terms of time course, relation to motor activity and state of vigilance. Using substantia nigra pars compacta lesions and both acute and chronic pharmacological interruptions of DA transmission, the present data demonstrated that the appearance of excessive beta synchronization requires a prolonged interruption in DA transmission and builds up progressively. This synchronization was vigilance-state dependent and observed solely during awake-like activity. Furthermore, these data demonstrated for the first time that the appearance of akinesia preceded the excessive cortical beta synchronization. In addition, this synchronization was stronger in the motor than in the somato-sensory cortex and in unilaterally compared with bilaterally lesioned animals. Finally, excessive beta synchronization was accompanied by an increased coherence between motor and somato-sensory cortical activities. These data suggest that excessive beta synchronization is associated with plastic processes whose time course is delayed with respect to the akinesia. Moreover, the expression of this phenomenon, which likely reflects functional changes in the cortico-basal ganglia circuits, requires a specific brain state.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Degos</LastName><ForeName>Bertrand</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Institut National de la Santé et de la Recherche Médicale U.667, Dynamique et Physiopathologie des Réseaux Neuronaux, Collège de France, 11 place Marcelin Berthelot, Paris Cedex 05, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deniau</LastName><ForeName>Jean-Michel</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Chavez</LastName><ForeName>Mario</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Maurice</LastName><ForeName>Nicolas</ForeName><Initials>N</Initials></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>2008</Year><Month>11</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cereb Cortex</MedlineTA><NlmUniqueID>9110718</NlmUniqueID><ISSNLinking>1047-3211</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001143" MajorTopicYN="Y">Arousal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001479" MajorTopicYN="N">Basal Ganglia</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001683" MajorTopicYN="Y">Biological Clocks</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002540" MajorTopicYN="N">Cerebral Cortex</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003344" MajorTopicYN="N">Cortical Synchronization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="Y">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017207" MajorTopicYN="N">Rats, Sprague-Dawley</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009435" MajorTopicYN="Y">Synaptic Transmission</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>11</Month><Day>11</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>8</Month><Day>27</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>11</Month><Day>11</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">18996909</ArticleId><ArticleId IdType="pii">bhn199</ArticleId><ArticleId IdType="doi">10.1093/cercor/bhn199</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country></list><tree><noCountry><name sortKey="Chavez, Mario" sort="Chavez, Mario" uniqKey="Chavez M" first="Mario" last="Chavez">Mario Chavez</name><name sortKey="Deniau, Jean Michel" sort="Deniau, Jean Michel" uniqKey="Deniau J" first="Jean-Michel" last="Deniau">Jean-Michel Deniau</name><name sortKey="Maurice, Nicolas" sort="Maurice, Nicolas" uniqKey="Maurice N" first="Nicolas" last="Maurice">Nicolas Maurice</name></noCountry><country name="France"><noRegion><name sortKey="Degos, Bertrand" sort="Degos, Bertrand" uniqKey="Degos B" first="Bertrand" last="Degos">Bertrand Degos</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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