Parkinsonian-like locomotor impairment in mice lacking dopamine D2 receptors.
Identifieur interne : 001614 ( PubMed/Corpus ); précédent : 001613; suivant : 001615Parkinsonian-like locomotor impairment in mice lacking dopamine D2 receptors.
Auteurs : J H Baik ; R. Picetti ; A. Saiardi ; G. Thiriet ; A. Dierich ; A. Depaulis ; M. Le Meur ; E. BorrelliSource :
- Nature [ 0028-0836 ] ; 1995.
English descriptors
- KwdEn :
- Animals, Brain (metabolism), Cell Line, Cloning, Molecular, Disease Models, Animal, Dopamine (metabolism), Female, In Situ Hybridization, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Motor Activity, Neuropeptides (biosynthesis), Neuropeptides (genetics), Ovary (metabolism), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), RNA (metabolism), Receptors, Dopamine D1 (metabolism), Receptors, Dopamine D2 (deficiency), Receptors, Dopamine D2 (physiology), Testis (metabolism).
- MESH :
- chemical , biosynthesis : Neuropeptides.
- chemical , deficiency : Receptors, Dopamine D2.
- chemical , genetics : Neuropeptides.
- chemical , metabolism : Dopamine, RNA, Receptors, Dopamine D1.
- metabolism : Brain, Ovary, Parkinson Disease, Testis.
- chemical , physiology : Receptors, Dopamine D2.
- physiopathology : Parkinson Disease.
- Animals, Cell Line, Cloning, Molecular, Disease Models, Animal, Female, In Situ Hybridization, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Motor Activity.
Abstract
Dopaminergic neuronal pathways arise from mesencephalic nuclei and project axons to the striatum, cortex, limbic system and hypothalamus. Through these pathways dopamine affects many physiological functions, such as the control of coordinated movement and hormone secretion. Here we have studied the physiological involvement of the dopamine D2 receptors in dopaminergic transmission, using homologous recombination to generate D2-receptor-deficient mice. Absence of D2 receptors leads to animals that are akinetic and bradykinetic in behavioural tests, and which show significantly reduced spontaneous movements. This phenotype presents analogies with symptoms characteristic of Parkinson's disease. Our study shows that D2 receptors have a key role in the dopaminergic control of nervous function. These mice have therapeutic potential as a model for investigating and correcting dysfunctions of the dopaminergic system.
DOI: 10.1038/377424a0
PubMed: 7566118
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Dierich</name></author><author><name sortKey="Depaulis, A" sort="Depaulis, A" uniqKey="Depaulis A" first="A" last="Depaulis">A. Depaulis</name></author><author><name sortKey="Le Meur, M" sort="Le Meur, M" uniqKey="Le Meur M" first="M" last="Le Meur">M. Le Meur</name></author><author><name sortKey="Borrelli, E" sort="Borrelli, E" uniqKey="Borrelli E" first="E" last="Borrelli">E. Borrelli</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1995">1995</date><idno type="RBID">pubmed:7566118</idno><idno type="pmid">7566118</idno><idno type="doi">10.1038/377424a0</idno><idno type="wicri:Area/PubMed/Corpus">001614</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001614</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Parkinsonian-like locomotor impairment in mice lacking dopamine D2 receptors.</title><author><name sortKey="Baik, J H" sort="Baik, J H" uniqKey="Baik J" first="J H" last="Baik">J H Baik</name><affiliation><nlm:affiliation>Institut de Génétique et de Biologíe Moléculaire et Cellulaire, Strasbourg, France.</nlm:affiliation></affiliation></author><author><name sortKey="Picetti, R" sort="Picetti, R" uniqKey="Picetti R" first="R" last="Picetti">R. Picetti</name></author><author><name sortKey="Saiardi, A" sort="Saiardi, A" uniqKey="Saiardi A" first="A" last="Saiardi">A. Saiardi</name></author><author><name sortKey="Thiriet, G" sort="Thiriet, G" uniqKey="Thiriet G" first="G" last="Thiriet">G. Thiriet</name></author><author><name sortKey="Dierich, A" sort="Dierich, A" uniqKey="Dierich A" first="A" last="Dierich">A. Dierich</name></author><author><name sortKey="Depaulis, A" sort="Depaulis, A" uniqKey="Depaulis A" first="A" last="Depaulis">A. Depaulis</name></author><author><name sortKey="Le Meur, M" sort="Le Meur, M" uniqKey="Le Meur M" first="M" last="Le Meur">M. Le Meur</name></author><author><name sortKey="Borrelli, E" sort="Borrelli, E" uniqKey="Borrelli E" first="E" last="Borrelli">E. Borrelli</name></author></analytic><series><title level="j">Nature</title><idno type="ISSN">0028-0836</idno><imprint><date when="1995" type="published">1995</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Brain (metabolism)</term><term>Cell Line</term><term>Cloning, Molecular</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Female</term><term>In Situ Hybridization</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Motor Activity</term><term>Neuropeptides (biosynthesis)</term><term>Neuropeptides (genetics)</term><term>Ovary (metabolism)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (physiopathology)</term><term>RNA (metabolism)</term><term>Receptors, Dopamine D1 (metabolism)</term><term>Receptors, Dopamine D2 (deficiency)</term><term>Receptors, Dopamine D2 (physiology)</term><term>Testis (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Neuropeptides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Neuropeptides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>RNA</term><term>Receptors, Dopamine D1</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Ovary</term><term>Parkinson Disease</term><term>Testis</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Cloning, Molecular</term><term>Disease Models, Animal</term><term>Female</term><term>In Situ Hybridization</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Motor Activity</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dopaminergic neuronal pathways arise from mesencephalic nuclei and project axons to the striatum, cortex, limbic system and hypothalamus. Through these pathways dopamine affects many physiological functions, such as the control of coordinated movement and hormone secretion. Here we have studied the physiological involvement of the dopamine D2 receptors in dopaminergic transmission, using homologous recombination to generate D2-receptor-deficient mice. Absence of D2 receptors leads to animals that are akinetic and bradykinetic in behavioural tests, and which show significantly reduced spontaneous movements. This phenotype presents analogies with symptoms characteristic of Parkinson's disease. Our study shows that D2 receptors have a key role in the dopaminergic control of nervous function. These mice have therapeutic potential as a model for investigating and correcting dysfunctions of the dopaminergic system.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">7566118</PMID><DateCreated><Year>1995</Year><Month>11</Month><Day>08</Day></DateCreated><DateCompleted><Year>1995</Year><Month>11</Month><Day>08</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0028-0836</ISSN><JournalIssue CitedMedium="Print"><Volume>377</Volume><Issue>6548</Issue><PubDate><Year>1995</Year><Month>Oct</Month><Day>05</Day></PubDate></JournalIssue><Title>Nature</Title><ISOAbbreviation>Nature</ISOAbbreviation></Journal><ArticleTitle>Parkinsonian-like locomotor impairment in mice lacking dopamine D2 receptors.</ArticleTitle><Pagination><MedlinePgn>424-8</MedlinePgn></Pagination><Abstract><AbstractText>Dopaminergic neuronal pathways arise from mesencephalic nuclei and project axons to the striatum, cortex, limbic system and hypothalamus. Through these pathways dopamine affects many physiological functions, such as the control of coordinated movement and hormone secretion. Here we have studied the physiological involvement of the dopamine D2 receptors in dopaminergic transmission, using homologous recombination to generate D2-receptor-deficient mice. Absence of D2 receptors leads to animals that are akinetic and bradykinetic in behavioural tests, and which show significantly reduced spontaneous movements. This phenotype presents analogies with symptoms characteristic of Parkinson's disease. Our study shows that D2 receptors have a key role in the dopaminergic control of nervous function. 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