Involvement of GABAA receptors in myoclonus
Identifieur interne : 004B84 ( Main/Exploration ); précédent : 004B83; suivant : 004B85Involvement of GABAA receptors in myoclonus
Auteurs : R. R. Matsumoto [États-Unis] ; D. D. Truong [États-Unis] ; K. D. Nguyen [États-Unis] ; A. T. Dang [États-Unis] ; T. T. Hoang [États-Unis] ; P. Q. Vo [États-Unis] ; P. Sandroni [États-Unis]Source :
- Movement disorders [ 0885-3185 ] ; 2000.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Animal, Animals, Brain Mapping, Caudate Nucleus (physiopathology), Cerebral Cortex (physiopathology), Epilepsies, Myoclonic (physiopathology), Experimental study, Gabaergic receptor A, Humans, Hypoxia, Brain (physiopathology), Intralaminar Thalamic Nuclei (physiopathology), Myoclonus, Myoclonus (physiopathology), Pathophysiology, Rat, Rats, Receptors, GABA-A (physiology).
- 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 GABAA 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. GABAA, but not GABAB, antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABAA antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABAA receptors at any one of a number of levels in the neural axis can produce myoclonus.
Affiliations:
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R." last="Matsumoto">R. R. Matsumoto</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>University of California Irvine, Department of Neurology</s1><s2>Irvine, California</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>University of Oklahoma Health Sciences Center, Department of Pharmacology & Toxicology</s1><s2>Oklahoma City, Oklahoma</s2><s3>USA</s3><sZ>1 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Oklahoma</region></placeName></affiliation></author><author><name sortKey="Truong, D D" sort="Truong, D D" uniqKey="Truong D" first="D. D." last="Truong">D. D. Truong</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>University of California Irvine, Department of Neurology</s1><s2>Irvine, California</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Long Beach Memorial Medical Center</s1><s2>Long Beach, California</s2><s3>USA</s3><sZ>2 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Nguyen, K D" sort="Nguyen, K D" uniqKey="Nguyen K" first="K. D." last="Nguyen">K. D. Nguyen</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>University of California Irvine, Department of Neurology</s1><s2>Irvine, California</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Dang, A T" sort="Dang, A T" uniqKey="Dang A" first="A. T." last="Dang">A. T. Dang</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>University of California Irvine, Department of Neurology</s1><s2>Irvine, California</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Hoang, T T" sort="Hoang, T T" uniqKey="Hoang T" first="T. T." last="Hoang">T. T. Hoang</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>University of California Irvine, Department of Neurology</s1><s2>Irvine, California</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Vo, P Q" sort="Vo, P Q" uniqKey="Vo P" first="P. Q." last="Vo">P. Q. Vo</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>University of California Irvine, Department of Neurology</s1><s2>Irvine, California</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Sandroni, P" sort="Sandroni, P" uniqKey="Sandroni P" first="P." last="Sandroni">P. Sandroni</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>University of California Irvine, Department of Neurology</s1><s2>Irvine, California</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation><affiliation wicri:level="2"><inist:fA14 i1="04"><s1>Mayo Clinic, Department of Neurology</s1><s2>Rochester, Minnesota</s2><s3>USA</s3><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Minnesota</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2000">2000</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term><term>Animals</term><term>Brain Mapping</term><term>Caudate Nucleus (physiopathology)</term><term>Cerebral Cortex (physiopathology)</term><term>Epilepsies, Myoclonic (physiopathology)</term><term>Experimental study</term><term>Gabaergic receptor A</term><term>Humans</term><term>Hypoxia, Brain (physiopathology)</term><term>Intralaminar Thalamic Nuclei (physiopathology)</term><term>Myoclonus</term><term>Myoclonus (physiopathology)</term><term>Pathophysiology</term><term>Rat</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><keywords scheme="Pascal" xml:lang="fr"><term>Myoclonie</term><term>Récepteur gabaergique A</term><term>Etude expérimentale</term><term>Physiopathologie</term><term>Animal</term><term>Rat</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<sub>A</sub> 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<sub>A</sub>, but not GABA<sub>B</sub>, antagonists produced myoclonus after microinjection into the NRT. Earlier investigators have further reported the ability of GABA<sub>A</sub> antagonists to produce myoclonus after microinjection into the caudate. The data therefore suggest that disruption of activity at GABA<sub>A</sub> receptors at any one of a number of levels in the neural axis can produce myoclonus.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li><li>Minnesota</li><li>Oklahoma</li></region></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Matsumoto, R R" sort="Matsumoto, R R" uniqKey="Matsumoto R" first="R. R." last="Matsumoto">R. R. Matsumoto</name></region><name sortKey="Dang, A T" sort="Dang, A T" uniqKey="Dang A" first="A. T." last="Dang">A. T. Dang</name><name sortKey="Hoang, T T" sort="Hoang, T T" uniqKey="Hoang T" first="T. T." last="Hoang">T. T. Hoang</name><name sortKey="Matsumoto, R R" sort="Matsumoto, R R" uniqKey="Matsumoto R" first="R. R." last="Matsumoto">R. R. Matsumoto</name><name sortKey="Nguyen, K D" sort="Nguyen, K D" uniqKey="Nguyen K" first="K. D." last="Nguyen">K. D. Nguyen</name><name sortKey="Sandroni, P" sort="Sandroni, P" uniqKey="Sandroni P" first="P." last="Sandroni">P. Sandroni</name><name sortKey="Sandroni, P" sort="Sandroni, P" uniqKey="Sandroni P" first="P." last="Sandroni">P. Sandroni</name><name sortKey="Truong, D D" sort="Truong, D D" uniqKey="Truong D" first="D. D." last="Truong">D. D. Truong</name><name sortKey="Truong, D D" sort="Truong, D D" uniqKey="Truong D" first="D. D." last="Truong">D. D. Truong</name><name sortKey="Vo, P Q" sort="Vo, P Q" uniqKey="Vo P" first="P. Q." last="Vo">P. Q. Vo</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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