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rdf:type |
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lifeskim:mentions |
umls-concept:C0013030,
umls-concept:C0013384,
umls-concept:C0034798,
umls-concept:C0037083,
umls-concept:C0057472,
umls-concept:C0086376,
umls-concept:C0206745,
umls-concept:C0332281,
umls-concept:C1419378,
umls-concept:C1514562,
umls-concept:C1704259,
umls-concept:C1704735,
umls-concept:C1705987,
umls-concept:C1710082,
umls-concept:C1880389,
umls-concept:C1883204,
umls-concept:C1883221
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pubmed:issue |
8
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pubmed:dateCreated |
2005-2-24
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pubmed:abstractText |
Regulator of G-protein signaling 9-2 (RGS9-2), a member of the RGS family of G GTPase accelerating proteins, is expressed specifically in the striatum, which participates in antipsychotic-induced tardive dyskinesia and in levodopa-induced dyskinesia. We report that RGS9 knock-out mice develop abnormal involuntary movements when inhibition of dopaminergic transmission is followed by activation of D2-like dopamine receptors (DRs). These abnormal movements resemble drug-induced dyskinesia more closely than other rodent models. Recordings from striatal neurons of these mice establish that activation of D2-like DRs abnormally inhibits glutamate-elicited currents. We show that RGS9-2, via its DEP domain (for Disheveled, EGL-10, Pleckstrin homology), colocalizes with D2DRs when coexpressed in mammalian cells. Recordings from oocytes coexpressing D2DR or the m2 muscarinic receptor and G-protein-gated inward rectifier potassium channels show that RGS9-2, via its DEP domain, preferentially accelerates the termination of D2DR signals. Thus, alterations in RGS9-2 may be a key factor in the pathway leading from D2DRs to the side effects associated with the treatment both of psychoses and Parkinson's disease.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2,3,4,5-Tetrahydro-7,8-dihydroxy-1-p...,
http://linkedlifedata.com/resource/pubmed/chemical/Antiparkinson Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Antipsychotic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Apomorphine,
http://linkedlifedata.com/resource/pubmed/chemical/Dopamine Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Dopamine Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Haloperidol,
http://linkedlifedata.com/resource/pubmed/chemical/Quinpirole,
http://linkedlifedata.com/resource/pubmed/chemical/RGS Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Dopamine D1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Dopamine D2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, G-Protein-Coupled,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Reserpine,
http://linkedlifedata.com/resource/pubmed/chemical/Sulpiride,
http://linkedlifedata.com/resource/pubmed/chemical/regulator of g-protein signaling 9
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1529-2401
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pubmed:author |
pubmed-author:AxelrodJeffrey DJD,
pubmed-author:BarghshoonSamiS,
pubmed-author:ChenChing-KangCK,
pubmed-author:CheyetteBenjamin N RBN,
pubmed-author:EbertJanaJ,
pubmed-author:KovoorAbrahamA,
pubmed-author:LesterHenry AHA,
pubmed-author:SchwarzJohannesJ,
pubmed-author:SchwarzSigridS,
pubmed-author:SeyffarthPetraP,
pubmed-author:SimonMelvin IMI
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pubmed:issnType |
Electronic
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pubmed:day |
23
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2157-65
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:15728856-2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine,
pubmed-meshheading:15728856-Animals,
pubmed-meshheading:15728856-Antiparkinson Agents,
pubmed-meshheading:15728856-Antipsychotic Agents,
pubmed-meshheading:15728856-Apomorphine,
pubmed-meshheading:15728856-Corpus Striatum,
pubmed-meshheading:15728856-Dopamine,
pubmed-meshheading:15728856-Dopamine Agents,
pubmed-meshheading:15728856-Dopamine Antagonists,
pubmed-meshheading:15728856-Dyskinesia, Drug-Induced,
pubmed-meshheading:15728856-Female,
pubmed-meshheading:15728856-Haloperidol,
pubmed-meshheading:15728856-Humans,
pubmed-meshheading:15728856-Mice,
pubmed-meshheading:15728856-Mice, Knockout,
pubmed-meshheading:15728856-Movement Disorders,
pubmed-meshheading:15728856-Parkinson Disease,
pubmed-meshheading:15728856-Patch-Clamp Techniques,
pubmed-meshheading:15728856-Protein Interaction Mapping,
pubmed-meshheading:15728856-Protein Structure, Tertiary,
pubmed-meshheading:15728856-Quinpirole,
pubmed-meshheading:15728856-RGS Proteins,
pubmed-meshheading:15728856-Receptors, Dopamine D1,
pubmed-meshheading:15728856-Receptors, Dopamine D2,
pubmed-meshheading:15728856-Receptors, G-Protein-Coupled,
pubmed-meshheading:15728856-Recombinant Fusion Proteins,
pubmed-meshheading:15728856-Reserpine,
pubmed-meshheading:15728856-Subcellular Fractions,
pubmed-meshheading:15728856-Sulpiride,
pubmed-meshheading:15728856-Transfection
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pubmed:year |
2005
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pubmed:articleTitle |
D2 dopamine receptors colocalize regulator of G-protein signaling 9-2 (RGS9-2) via the RGS9 DEP domain, and RGS9 knock-out mice develop dyskinesias associated with dopamine pathways.
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pubmed:affiliation |
Division of Biology, California Institute of Technology, Pasadena, California 91125, USA.
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pubmed:publicationType |
Journal Article
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