Impaired locomotion and dopamine signaling in retinoid receptor mutant mice.
Identifieur interne : 001342 ( PubMed/Checkpoint ); précédent : 001341; suivant : 001343Impaired locomotion and dopamine signaling in retinoid receptor mutant mice.
Auteurs : W. Krezel [France] ; N. Ghyselinck ; T A Samad ; V. Dupé ; P. Kastner ; E. Borrelli ; P. ChambonSource :
- Science (New York, N.Y.) [ 0036-8075 ] ; 1998.
English descriptors
- KwdEn :
- Animals, Cocaine (pharmacology), Corpus Striatum (metabolism), Dimerization, Dopamine (metabolism), Locomotion, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Motor Activity (drug effects), Muscle, Skeletal (physiology), Parkinson Disease (etiology), Peripheral Nervous System (physiology), Receptors, Dopamine D1 (genetics), Receptors, Dopamine D1 (metabolism), Receptors, Dopamine D2 (genetics), Receptors, Dopamine D2 (metabolism), Receptors, Retinoic Acid (genetics), Receptors, Retinoic Acid (physiology), Retinoid X Receptors, Schizophrenia (etiology), Signal Transduction, Transcription Factors (genetics), Transcription Factors (physiology).
- MESH :
- chemical , genetics : Receptors, Dopamine D1, Receptors, Dopamine D2, Receptors, Retinoic Acid, Transcription Factors.
- chemical , metabolism : Dopamine, Receptors, Dopamine D1, Receptors, Dopamine D2.
- chemical , pharmacology : Cocaine.
- drug effects : Motor Activity.
- etiology : Parkinson Disease, Schizophrenia.
- metabolism : Corpus Striatum.
- physiology : Muscle, Skeletal, Peripheral Nervous System, Receptors, Retinoic Acid, Transcription Factors.
- Animals, Dimerization, Locomotion, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Retinoid X Receptors, Signal Transduction.
Abstract
In the adult mouse, single and compound null mutations in the genes for retinoic acid receptor beta and retinoid X receptors beta and gamma resulted in locomotor defects related to dysfunction of the mesolimbic dopamine signaling pathway. Expression of the D1 and D2 receptors for dopamine was reduced in the ventral striatum of mutant mice, and the response of double null mutant mice to cocaine, which affects dopamine signaling in the mesolimbic system, was blunted. Thus, retinoid receptors are involved in the regulation of brain functions, and retinoic acid signaling defects may contribute to pathologies such as Parkinson's disease and schizophrenia.
PubMed: 9452386
Affiliations:
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Krezel</name><affiliation wicri:level="4"><nlm:affiliation>Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS, INSERM, Université Louis Pasteur, Collège de France, Boite Postale 163, 67404 Illkirch Cedex, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS, INSERM, Université Louis Pasteur, Collège de France, Boite Postale 163, 67404 Illkirch Cedex</wicri:regionArea><placeName><region type="region" nuts="2">Grand Est</region><region type="old region" nuts="2">Alsace (région administrative)</region><settlement type="city">Illkirch</settlement></placeName><orgName type="university">Université Strasbourg 1</orgName></affiliation></author><author><name sortKey="Ghyselinck, N" sort="Ghyselinck, N" uniqKey="Ghyselinck N" first="N" last="Ghyselinck">N. 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Chambon</name></author></analytic><series><title level="j">Science (New York, N.Y.)</title><idno type="ISSN">0036-8075</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cocaine (pharmacology)</term><term>Corpus Striatum (metabolism)</term><term>Dimerization</term><term>Dopamine (metabolism)</term><term>Locomotion</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Motor Activity (drug effects)</term><term>Muscle, Skeletal (physiology)</term><term>Parkinson Disease (etiology)</term><term>Peripheral Nervous System (physiology)</term><term>Receptors, Dopamine D1 (genetics)</term><term>Receptors, Dopamine D1 (metabolism)</term><term>Receptors, Dopamine D2 (genetics)</term><term>Receptors, Dopamine D2 (metabolism)</term><term>Receptors, Retinoic Acid (genetics)</term><term>Receptors, Retinoic Acid (physiology)</term><term>Retinoid X Receptors</term><term>Schizophrenia (etiology)</term><term>Signal Transduction</term><term>Transcription Factors (genetics)</term><term>Transcription Factors (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, Dopamine D1</term><term>Receptors, Dopamine D2</term><term>Receptors, Retinoic Acid</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Receptors, Dopamine D1</term><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Cocaine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Muscle, Skeletal</term><term>Peripheral Nervous System</term><term>Receptors, Retinoic Acid</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Dimerization</term><term>Locomotion</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Retinoid X Receptors</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the adult mouse, single and compound null mutations in the genes for retinoic acid receptor beta and retinoid X receptors beta and gamma resulted in locomotor defects related to dysfunction of the mesolimbic dopamine signaling pathway. Expression of the D1 and D2 receptors for dopamine was reduced in the ventral striatum of mutant mice, and the response of double null mutant mice to cocaine, which affects dopamine signaling in the mesolimbic system, was blunted. Thus, retinoid receptors are involved in the regulation of brain functions, and retinoic acid signaling defects may contribute to pathologies such as Parkinson's disease and schizophrenia.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9452386</PMID><DateCreated><Year>1998</Year><Month>02</Month><Day>23</Day></DateCreated><DateCompleted><Year>1998</Year><Month>02</Month><Day>23</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0036-8075</ISSN><JournalIssue CitedMedium="Print"><Volume>279</Volume><Issue>5352</Issue><PubDate><Year>1998</Year><Month>Feb</Month><Day>06</Day></PubDate></JournalIssue><Title>Science (New York, N.Y.)</Title><ISOAbbreviation>Science</ISOAbbreviation></Journal><ArticleTitle>Impaired locomotion and dopamine signaling in retinoid receptor mutant mice.</ArticleTitle><Pagination><MedlinePgn>863-7</MedlinePgn></Pagination><Abstract><AbstractText>In the adult mouse, single and compound null mutations in the genes for retinoic acid receptor beta and retinoid X receptors beta and gamma resulted in locomotor defects related to dysfunction of the mesolimbic dopamine signaling pathway. Expression of the D1 and D2 receptors for dopamine was reduced in the ventral striatum of mutant mice, and the response of double null mutant mice to cocaine, which affects dopamine signaling in the mesolimbic system, was blunted. Thus, retinoid receptors are involved in the regulation of brain functions, and retinoic acid signaling defects may contribute to pathologies such as Parkinson's disease and schizophrenia.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Krezel</LastName><ForeName>W</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS, INSERM, Université Louis Pasteur, Collège de France, Boite Postale 163, 67404 Illkirch Cedex, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ghyselinck</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Samad</LastName><ForeName>T A</ForeName><Initials>TA</Initials></Author><Author ValidYN="Y"><LastName>Dupé</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Kastner</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Borrelli</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Chambon</LastName><ForeName>P</ForeName><Initials>P</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>Science</MedlineTA><NlmUniqueID>0404511</NlmUniqueID><ISSNLinking>0036-8075</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017447">Receptors, Dopamine D1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017448">Receptors, Dopamine D2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018168">Receptors, Retinoic 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1</li></orgName></list><tree><noCountry><name sortKey="Borrelli, E" sort="Borrelli, E" uniqKey="Borrelli E" first="E" last="Borrelli">E. Borrelli</name><name sortKey="Chambon, P" sort="Chambon, P" uniqKey="Chambon P" first="P" last="Chambon">P. Chambon</name><name sortKey="Dupe, V" sort="Dupe, V" uniqKey="Dupe V" first="V" last="Dupé">V. Dupé</name><name sortKey="Ghyselinck, N" sort="Ghyselinck, N" uniqKey="Ghyselinck N" first="N" last="Ghyselinck">N. Ghyselinck</name><name sortKey="Kastner, P" sort="Kastner, P" uniqKey="Kastner P" first="P" last="Kastner">P. Kastner</name><name sortKey="Samad, T A" sort="Samad, T A" uniqKey="Samad T" first="T A" last="Samad">T A Samad</name></noCountry><country name="France"><region name="Grand Est"><name sortKey="Krezel, W" sort="Krezel, W" uniqKey="Krezel W" first="W" last="Krezel">W. Krezel</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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