Prevention of levodopa-induced dyskinesias by a selective NR1A/2B N-methyl-D-aspartate receptor antagonist in parkinsonian monkeys: implication of preproenkephalin.
Identifieur interne : 000569 ( Ncbi/Merge ); précédent : 000568; suivant : 000570Prevention of levodopa-induced dyskinesias by a selective NR1A/2B N-methyl-D-aspartate receptor antagonist in parkinsonian monkeys: implication of preproenkephalin.
Auteurs : Marc Morissette [Canada] ; Mehdi Dridi ; Frédéric Calon ; Abdallah Hadj Tahar ; Leonard T. Meltzer ; Paul J. Bédard ; Thérèse Di PaoloSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2006.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (toxicity), Benserazide (toxicity), Benzoxazoles (pharmacology), Corpus Striatum (drug effects), Corpus Striatum (pathology), Corpus Striatum (physiopathology), Dopamine (metabolism), Drug Therapy, Combination, Dyskinesia, Drug-Induced (pathology), Dyskinesia, Drug-Induced (physiopathology), Enkephalins (genetics), Enkephalins (physiology), Female, Gene Expression (drug effects), Levodopa (toxicity), Macaca fascicularis, Parkinsonian Disorders (pathology), Parkinsonian Disorders (physiopathology), Piperidines (pharmacology), Protein Precursors (genetics), Protein Precursors (physiology), RNA, Messenger (genetics), Receptors, N-Methyl-D-Aspartate (antagonists & inhibitors).
- MESH :
- chemical , antagonists & inhibitors : Receptors, N-Methyl-D-Aspartate.
- chemical , genetics : Enkephalins, Protein Precursors, RNA, Messenger.
- chemical , metabolism : Dopamine.
- chemical , pharmacology : Benzoxazoles, Piperidines.
- chemical , physiology : Enkephalins, Protein Precursors.
- chemical , toxicity : Antiparkinson Agents, Benserazide, Levodopa.
- drug effects : Corpus Striatum, Gene Expression.
- pathology : Corpus Striatum, Dyskinesia, Drug-Induced, Parkinsonian Disorders.
- physiopathology : Corpus Striatum, Dyskinesia, Drug-Induced, Parkinsonian Disorders.
- Animals, Drug Therapy, Combination, Female, Macaca fascicularis.
Abstract
Enkephalin is reported to play an important role in the pathophysiology of levodopa (LD) -induced dyskinesias. The present study investigated the effect of chronic treatment with a selective NR1A/2B N-methyl-D-aspartate (NMDA) receptor antagonist, CI-1041, on the expression of preproenkephalin-A (PPE-A) in brains of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) -treated monkeys in relation to the development of LD-induced dyskinesias. Four MPTP-monkeys received LD/benserazide alone; they all developed dyskinesias. Four other MPTP-monkeys received LD/benserazide plus CI-1041; only one of them developed mild dyskinesias at the end of the fourth week of treatment. Four normal monkeys and four saline-treated MPTP monkeys were also included. MPTP-treated monkeys had extensive and similar striatal dopamine denervation. An increase of PPE-A mRNA levels assayed by in situ hybridization was observed in the lateral putamen (rostral and caudal) and caudate nucleus (rostral) of saline-treated MPTP monkeys compared to controls, whereas no change or a small increase was observed in their medial parts. Striatal PPE-A mRNA levels remained elevated in LD-treated MPTP monkeys, whereas cotreatment with CI-1041 brought them back to control values. These findings suggest that chronic blockade of striatal NR1A/2B NMDA receptors with CI-1041 normalizes PPE-A mRNA expression and prevents the development of LD-induced dyskinesias in an animal model of Parkinson disease.
DOI: 10.1002/mds.20654
PubMed: 16127720
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pubmed:16127720Le document en format XML
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Meltzer</name></author><author><name sortKey="Bedard, Paul J" sort="Bedard, Paul J" uniqKey="Bedard P" first="Paul J" last="Bédard">Paul J. Bédard</name></author><author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</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="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (toxicity)</term><term>Benserazide (toxicity)</term><term>Benzoxazoles (pharmacology)</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (pathology)</term><term>Corpus Striatum (physiopathology)</term><term>Dopamine (metabolism)</term><term>Drug Therapy, Combination</term><term>Dyskinesia, Drug-Induced (pathology)</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Enkephalins (genetics)</term><term>Enkephalins (physiology)</term><term>Female</term><term>Gene Expression (drug effects)</term><term>Levodopa (toxicity)</term><term>Macaca fascicularis</term><term>Parkinsonian Disorders (pathology)</term><term>Parkinsonian Disorders (physiopathology)</term><term>Piperidines (pharmacology)</term><term>Protein Precursors (genetics)</term><term>Protein Precursors (physiology)</term><term>RNA, Messenger (genetics)</term><term>Receptors, N-Methyl-D-Aspartate (antagonists & inhibitors)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, N-Methyl-D-Aspartate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Enkephalins</term><term>Protein Precursors</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Benzoxazoles</term><term>Piperidines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Enkephalins</term><term>Protein Precursors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Antiparkinson Agents</term><term>Benserazide</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Corpus Striatum</term><term>Gene Expression</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>Dyskinesia, Drug-Induced</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term><term>Dyskinesia, Drug-Induced</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Drug Therapy, Combination</term><term>Female</term><term>Macaca fascicularis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Enkephalin is reported to play an important role in the pathophysiology of levodopa (LD) -induced dyskinesias. The present study investigated the effect of chronic treatment with a selective NR1A/2B N-methyl-D-aspartate (NMDA) receptor antagonist, CI-1041, on the expression of preproenkephalin-A (PPE-A) in brains of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) -treated monkeys in relation to the development of LD-induced dyskinesias. Four MPTP-monkeys received LD/benserazide alone; they all developed dyskinesias. Four other MPTP-monkeys received LD/benserazide plus CI-1041; only one of them developed mild dyskinesias at the end of the fourth week of treatment. Four normal monkeys and four saline-treated MPTP monkeys were also included. MPTP-treated monkeys had extensive and similar striatal dopamine denervation. An increase of PPE-A mRNA levels assayed by in situ hybridization was observed in the lateral putamen (rostral and caudal) and caudate nucleus (rostral) of saline-treated MPTP monkeys compared to controls, whereas no change or a small increase was observed in their medial parts. Striatal PPE-A mRNA levels remained elevated in LD-treated MPTP monkeys, whereas cotreatment with CI-1041 brought them back to control values. These findings suggest that chronic blockade of striatal NR1A/2B NMDA receptors with CI-1041 normalizes PPE-A mRNA expression and prevents the development of LD-induced dyskinesias in an animal model of Parkinson disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16127720</PMID><DateCreated><Year>2006</Year><Month>01</Month><Day>19</Day></DateCreated><DateCompleted><Year>2006</Year><Month>07</Month><Day>03</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>21</Volume><Issue>1</Issue><PubDate><Year>2006</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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Four normal monkeys and four saline-treated MPTP monkeys were also included. MPTP-treated monkeys had extensive and similar striatal dopamine denervation. An increase of PPE-A mRNA levels assayed by in situ hybridization was observed in the lateral putamen (rostral and caudal) and caudate nucleus (rostral) of saline-treated MPTP monkeys compared to controls, whereas no change or a small increase was observed in their medial parts. Striatal PPE-A mRNA levels remained elevated in LD-treated MPTP monkeys, whereas cotreatment with CI-1041 brought them back to control values. These findings suggest that chronic blockade of striatal NR1A/2B NMDA receptors with CI-1041 normalizes PPE-A mRNA expression and prevents the development of LD-induced dyskinesias in an animal model of Parkinson disease.</AbstractText><CopyrightInformation>Copyright (c) 2005 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Morissette</LastName><ForeName>Marc</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Molecular Endocrinology and Oncology Research Centre, Laval University Medical Centre, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dridi</LastName><ForeName>Mehdi</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Calon</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Hadj Tahar</LastName><ForeName>Abdallah</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Meltzer</LastName><ForeName>Leonard T</ForeName><Initials>LT</Initials></Author><Author ValidYN="Y"><LastName>Bédard</LastName><ForeName>Paul J</ForeName><Initials>PJ</Initials></Author><Author ValidYN="Y"><LastName>Di Paolo</LastName><ForeName>Thérèse</ForeName><Initials>T</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></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="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>5K3N2D15WW</RegistryNumber><NameOfSubstance UI="C481484">besonprodil</NameOfSubstance></Chemical><Chemical><RegistryNumber>762OS3ZEJU</RegistryNumber><NameOfSubstance UI="D001545">Benserazide</NameOfSubstance></Chemical><Chemical><RegistryNumber>93443-35-7</RegistryNumber><NameOfSubstance UI="C033660">preproenkephalin</NameOfSubstance></Chemical><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="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001545" MajorTopicYN="N">Benserazide</DescriptorName><QualifierName 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Bédard</name><name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric Calon</name><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name><name sortKey="Dridi, Mehdi" sort="Dridi, Mehdi" uniqKey="Dridi M" first="Mehdi" last="Dridi">Mehdi Dridi</name><name sortKey="Hadj Tahar, Abdallah" sort="Hadj Tahar, Abdallah" uniqKey="Hadj Tahar A" first="Abdallah" last="Hadj Tahar">Abdallah Hadj Tahar</name><name sortKey="Meltzer, Leonard T" sort="Meltzer, Leonard T" uniqKey="Meltzer L" first="Leonard T" last="Meltzer">Leonard T. Meltzer</name></noCountry><country name="Canada"><noRegion><name sortKey="Morissette, Marc" sort="Morissette, Marc" uniqKey="Morissette M" first="Marc" last="Morissette">Marc Morissette</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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