Involvement of GABA(A) receptors in myoclonus.
Identifieur interne : 003F90 ( PubMed/Corpus ); précédent : 003F89; suivant : 003F91Involvement of GABA(A) receptors in myoclonus.
Auteurs : R R Matsumoto ; D D Truong ; K D Nguyen ; A T Dang ; T T Hoang ; P Q Vo ; P. SandroniSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2000.
English descriptors
- KwdEn :
- MESH :
- chemical , physiology : Receptors, GABA-A.
- physiopathology : Caudate Nucleus, Cerebral Cortex, Epilepsies, Myoclonic, Hypoxia, Brain, Intralaminar Thalamic Nuclei, Myoclonus.
- Animals, Brain Mapping, Humans, Rats.
Abstract
Alterations in multiple neurochemical systems have been reported in animal and human studies of posthypoxic myoclonus. It is impossible, however, to establish causative relationships between the observed changes and the myoclonic movements from these studies. Therefore, to establish causative links between neurochemical changes and myoclonus, ligands that target neurotransmitter systems that are altered in posthypoxic myoclonus were microinjected into the lateral ventricles of normal rats to identify the changes that can produce myoclonus. Of the ligands that were tested, only the GABA(A) antagonists produced myoclonus after intracerebroventricular administration, suggesting the importance of disinhibition of GABAergic systems in myoclonus. To further examine the role of GABA in myoclonus, GABAergic antagonists were microinjected into the nucleus reticularis of the thalamus (NRT), an area of the brain in which extensive pathologic changes are seen in posthypoxic animals. GABA(A), but not GABA(B), antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABA(A) antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABA(A) receptors at any one of a number of levels in the neural axis can produce myoclonus.
PubMed: 10755272
Links to Exploration step
pubmed:10755272Le document en format XML
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Sandroni</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2000">2000</date><idno type="RBID">pubmed:10755272</idno><idno type="pmid">10755272</idno><idno type="wicri:Area/PubMed/Corpus">003F90</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Involvement of GABA(A) receptors in myoclonus.</title><author><name sortKey="Matsumoto, R R" sort="Matsumoto, R R" uniqKey="Matsumoto R" first="R R" last="Matsumoto">R R Matsumoto</name><affiliation><nlm:affiliation>University of California Irvine, Department of Neorology, California, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Truong, D D" sort="Truong, D D" uniqKey="Truong D" first="D D" last="Truong">D D Truong</name></author><author><name sortKey="Nguyen, K D" sort="Nguyen, K D" uniqKey="Nguyen K" first="K D" last="Nguyen">K D Nguyen</name></author><author><name sortKey="Dang, A T" sort="Dang, A T" uniqKey="Dang A" first="A T" last="Dang">A T Dang</name></author><author><name sortKey="Hoang, T T" sort="Hoang, T T" uniqKey="Hoang T" first="T T" last="Hoang">T T Hoang</name></author><author><name sortKey="Vo, P Q" sort="Vo, P Q" uniqKey="Vo P" first="P Q" last="Vo">P Q Vo</name></author><author><name sortKey="Sandroni, P" sort="Sandroni, P" uniqKey="Sandroni P" first="P" last="Sandroni">P. Sandroni</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Brain Mapping</term><term>Caudate Nucleus (physiopathology)</term><term>Cerebral Cortex (physiopathology)</term><term>Epilepsies, Myoclonic (physiopathology)</term><term>Humans</term><term>Hypoxia, Brain (physiopathology)</term><term>Intralaminar Thalamic Nuclei (physiopathology)</term><term>Myoclonus (physiopathology)</term><term>Rats</term><term>Receptors, GABA-A (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, GABA-A</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Caudate Nucleus</term><term>Cerebral Cortex</term><term>Epilepsies, Myoclonic</term><term>Hypoxia, Brain</term><term>Intralaminar Thalamic Nuclei</term><term>Myoclonus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Brain Mapping</term><term>Humans</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alterations in multiple neurochemical systems have been reported in animal and human studies of posthypoxic myoclonus. It is impossible, however, to establish causative relationships between the observed changes and the myoclonic movements from these studies. Therefore, to establish causative links between neurochemical changes and myoclonus, ligands that target neurotransmitter systems that are altered in posthypoxic myoclonus were microinjected into the lateral ventricles of normal rats to identify the changes that can produce myoclonus. Of the ligands that were tested, only the GABA(A) antagonists produced myoclonus after intracerebroventricular administration, suggesting the importance of disinhibition of GABAergic systems in myoclonus. To further examine the role of GABA in myoclonus, GABAergic antagonists were microinjected into the nucleus reticularis of the thalamus (NRT), an area of the brain in which extensive pathologic changes are seen in posthypoxic animals. GABA(A), but not GABA(B), antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABA(A) antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABA(A) receptors at any one of a number of levels in the neural axis can produce myoclonus.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">10755272</PMID><DateCreated><Year>2000</Year><Month>05</Month><Day>25</Day></DateCreated><DateCompleted><Year>2000</Year><Month>05</Month><Day>25</Day></DateCompleted><DateRevised><Year>2005</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>15 Suppl 1</Volume><PubDate><Year>2000</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Involvement of GABA(A) receptors in myoclonus.</ArticleTitle><Pagination><MedlinePgn>47-52</MedlinePgn></Pagination><Abstract><AbstractText>Alterations in multiple neurochemical systems have been reported in animal and human studies of posthypoxic myoclonus. It is impossible, however, to establish causative relationships between the observed changes and the myoclonic movements from these studies. Therefore, to establish causative links between neurochemical changes and myoclonus, ligands that target neurotransmitter systems that are altered in posthypoxic myoclonus were microinjected into the lateral ventricles of normal rats to identify the changes that can produce myoclonus. Of the ligands that were tested, only the GABA(A) antagonists produced myoclonus after intracerebroventricular administration, suggesting the importance of disinhibition of GABAergic systems in myoclonus. To further examine the role of GABA in myoclonus, GABAergic antagonists were microinjected into the nucleus reticularis of the thalamus (NRT), an area of the brain in which extensive pathologic changes are seen in posthypoxic animals. GABA(A), but not GABA(B), antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABA(A) antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABA(A) receptors at any one of a number of levels in the neural axis can produce myoclonus.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Matsumoto</LastName><ForeName>R R</ForeName><Initials>RR</Initials><AffiliationInfo><Affiliation>University of California Irvine, Department of Neorology, California, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Truong</LastName><ForeName>D D</ForeName><Initials>DD</Initials></Author><Author ValidYN="Y"><LastName>Nguyen</LastName><ForeName>K D</ForeName><Initials>KD</Initials></Author><Author ValidYN="Y"><LastName>Dang</LastName><ForeName>A T</ForeName><Initials>AT</Initials></Author><Author ValidYN="Y"><LastName>Hoang</LastName><ForeName>T T</ForeName><Initials>TT</Initials></Author><Author ValidYN="Y"><LastName>Vo</LastName><ForeName>P Q</ForeName><Initials>PQ</Initials></Author><Author ValidYN="Y"><LastName>Sandroni</LastName><ForeName>P</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011963">Receptors, GABA-A</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001931">Brain Mapping</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002421">Caudate Nucleus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002540">Cerebral Cortex</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004831">Epilepsies, Myoclonic</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002534">Hypoxia, Brain</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020646">Intralaminar Thalamic Nuclei</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009207">Myoclonus</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011963">Receptors, GABA-A</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>27</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>4</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>6</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>4</Month><Day>8</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10755272</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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