Pathogenesis of levodopa-induced dyskinesia: focus on D1 and D3 dopamine receptors.
Identifieur interne : 002F24 ( Main/Merge ); précédent : 002F23; suivant : 002F25Pathogenesis of levodopa-induced dyskinesia: focus on D1 and D3 dopamine receptors.
Auteurs : C. Guigoni [France] ; I. Aubert ; Q. Li ; V V Gurevich ; J L Benovic ; S. Ferry ; U. Mach ; H. Stark ; L. Leriche ; K. H Kansson ; Bernard H. Bioulac ; Christian E. Gross ; Pierre Sokoloff ; Gilberto Fisone ; E V Gurevich ; Bertrand Bloch ; Erwan BezardSource :
- Parkinsonism & related disorders [ 1353-8020 ] ; 2005.
English descriptors
- KwdEn :
- Antiparkinson Agents (adverse effects), Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (physiopathology), Humans, Levodopa (adverse effects), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Receptors, Dopamine D1 (physiology), Receptors, Dopamine D2 (physiology), Receptors, Dopamine D3.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- chemical , physiology : Receptors, Dopamine D1, Receptors, Dopamine D2.
- physiopathology : Dyskinesia, Drug-Induced, Parkinson Disease.
- Humans, Receptors, Dopamine D3.
Abstract
Involuntary movements, or dyskinesia, represent a debilitating complication of levodopa therapy for Parkinson's disease. Taking advantage of a monkey brain bank constituted to study the pathophysiology of levodopa-induced dyskinesia, we here report the changes affecting D1, D2 and D3 dopamine receptors within the striatum of four experimental groups of non-human primates: normal, parkinsonian, parkinsonian treated with levodopa without or with dyskinesia. We also report the possible role of arrestin and G protein-coupled receptor kinases.
DOI: 10.1016/j.parkreldis.2004.11.005
PubMed: 15885624
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pubmed:15885624Le document en format XML
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Taking advantage of a monkey brain bank constituted to study the pathophysiology of levodopa-induced dyskinesia, we here report the changes affecting D1, D2 and D3 dopamine receptors within the striatum of four experimental groups of non-human primates: normal, parkinsonian, parkinsonian treated with levodopa without or with dyskinesia. We also report the possible role of arrestin and G protein-coupled receptor kinases.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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