Movement Disorders (revue)

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Animal model of posthypoxic myoclonus: II. Neurochemical, pathologic, and pharmacologic characterization

Identifieur interne : 001E00 ( Istex/Corpus ); précédent : 001D99; suivant : 001E01

Animal model of posthypoxic myoclonus: II. Neurochemical, pathologic, and pharmacologic characterization

Auteurs : Anumantha G. Kanthasamy ; Bang Q. Nguyen ; Daniel D. Truong

Source :

RBID : ISTEX:9F594A31A342D2B1A5794ED146A3F6402F6B2266

English descriptors

Abstract

The sudden, brief, shock‐like, involuntary movements caused by active muscular contractions or inhibitions characterize myoclonus. It is manifested in a wide variety of pathologic conditions affecting the brain, spinal cord, or peripheral nerves, and is thought to be related to neuronal hyper‐excitability. The pathology, physiology, and pharmacology of myoclonus are not well understood as a result of the rarity of the disorder in people and the lack of a suitable animal model. Posthypoxic myoclonus is a major myoclonus syndrome which occurs as a result of severe cerebral ischemia/hypoxia. There has been tremendous interest in the development of a suitable animal model that reflects the etiology and clinical pathology of posthypoxic myoclonus. Recently, we have developed a new animal model of posthypoxic myoclonus in which rats were subjected to a mechanically induced cardiac arrest procedure. Herein, we describe the neurochemical, pharmacologic, and pathologic characteristics of this animal model of posthypoxic myoclonus.

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DOI: 10.1002/mds.870150707

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ISTEX:9F594A31A342D2B1A5794ED146A3F6402F6B2266

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<title>Animal model of posthypoxic myoclonus: II. Neurochemical, pathologic, and pharmacologic characterization</title>
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<titleInfo type="abbreviated" lang="en">
<title>NEUROCHEMICAL, PATHOLOGIC, AND PHARMACOLOGIC CHARACTERIZATION</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA" lang="en">
<title>Animal model of posthypoxic myoclonus: II. Neurochemical, pathologic, and pharmacologic characterization</title>
</titleInfo>
<name type="personal">
<namePart type="given">Anumantha G.</namePart>
<namePart type="family">Kanthasamy</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>The Parkinson's and Movement Disorder Institute, Long Beach Memorial Medical Center, Long Beach, California, U.S.A.</affiliation>
<affiliation>Orange Coast Memorial Medical Center, Fountain Valley, California, U.S.A.</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Bang Q.</namePart>
<namePart type="family">Nguyen</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>The Parkinson's and Movement Disorder Institute, Long Beach Memorial Medical Center, Long Beach, California, U.S.A.</affiliation>
<affiliation>Orange Coast Memorial Medical Center, Fountain Valley, California, U.S.A.</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">Daniel D.</namePart>
<namePart type="family">Truong</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>The Parkinson's and Movement Disorder Institute, Long Beach Memorial Medical Center, Long Beach, California, U.S.A.</affiliation>
<affiliation>Orange Coast Memorial Medical Center, Fountain Valley, California, U.S.A.</affiliation>
<description>Correspondence: The Parkinson and Movement Disorder Institute, 9900 Talbert Ave, #200, Fountain Valley, CA 92708, U.S.A.</description>
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<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<place>
<placeTerm type="text">Hoboken</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2000-09</dateIssued>
<copyrightDate encoding="w3cdtf">2000</copyrightDate>
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<languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<extent unit="figures">6</extent>
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<abstract lang="en">The sudden, brief, shock‐like, involuntary movements caused by active muscular contractions or inhibitions characterize myoclonus. It is manifested in a wide variety of pathologic conditions affecting the brain, spinal cord, or peripheral nerves, and is thought to be related to neuronal hyper‐excitability. The pathology, physiology, and pharmacology of myoclonus are not well understood as a result of the rarity of the disorder in people and the lack of a suitable animal model. Posthypoxic myoclonus is a major myoclonus syndrome which occurs as a result of severe cerebral ischemia/hypoxia. There has been tremendous interest in the development of a suitable animal model that reflects the etiology and clinical pathology of posthypoxic myoclonus. Recently, we have developed a new animal model of posthypoxic myoclonus in which rats were subjected to a mechanically induced cardiac arrest procedure. Herein, we describe the neurochemical, pharmacologic, and pathologic characteristics of this animal model of posthypoxic myoclonus.</abstract>
<note type="funding">Myoclonus Research Foundation</note>
<note type="funding">NIH‐SACNAS Biomedical Research</note>
<subject lang="en">
<genre>Keywords</genre>
<topic>Myoclonus</topic>
<topic>Animal model</topic>
<topic>Hypoxia</topic>
<topic>Movement disorder</topic>
<topic>Cardiac arrest</topic>
<topic>Serotonin</topic>
<topic>DDT</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>Movement Disorders</title>
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<titleInfo type="abbreviated">
<title>Mov. Disord.</title>
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<genre>article category</genre>
<topic>Article</topic>
</subject>
<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part>
<date>2000</date>
<detail type="volume">
<caption>vol.</caption>
<number>15</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>S1</number>
</detail>
<detail type="supplement">
<caption>Suppl. no.</caption>
<number>S1</number>
</detail>
<extent unit="pages">
<start>31</start>
<end>38</end>
<total>8</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">9F594A31A342D2B1A5794ED146A3F6402F6B2266</identifier>
<identifier type="DOI">10.1002/mds.870150707</identifier>
<identifier type="ArticleID">MDS870150707</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2000 Movement Disorder Society</accessCondition>
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