Involvement of sensorimotor, limbic, and associative basal ganglia domains in L-3,4-dihydroxyphenylalanine-induced dyskinesia

Dyskinesia represents a debilitating complication of L-3,4-dihydroxyphenylalanine (L-dopa) therapy for Parkinson's disease. Such motor manifestations are attributed to pathological activity in the motor parts of basal ganglia. However, because consistent funneling of information takes place bet...

Celý popis

Uložené v:
Podrobná bibliografia
Vydané v:The Journal of neuroscience Ročník 25; číslo 8; s. 2102
Hlavní autori: Guigoni, Céline, Li, Qin, Aubert, Incarnation, Dovero, Sandra, Bioulac, Bernard H, Bloch, Bertrand, Crossman, Alan R, Gross, Christian E, Bezard, Erwan
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 23.02.2005
Predmet:
Animals
Basal Ganglia - chemistry
Basal Ganglia - physiopathology
Deoxyglucose - pharmacokinetics
Dyskinesia, Drug-Induced - metabolism
Dyskinesia, Drug-Induced - physiopathology
Female
Globus Pallidus - chemistry
Globus Pallidus - physiopathology
Levodopa - therapeutic use
Levodopa - toxicity
Limbic System - chemistry
Limbic System - physiopathology
Macaca fascicularis
Motor Cortex - chemistry
Motor Cortex - physiopathology
Parkinsonian Disorders - drug therapy
Parkinsonian Disorders - physiopathology
Septal Nuclei - chemistry
Septal Nuclei - physiopathology
Somatosensory Cortex - chemistry
Somatosensory Cortex - physiopathology
Substantia Nigra - chemistry
Substantia Nigra - physiopathology
Subthalamic Nucleus - chemistry
Subthalamic Nucleus - physiopathology
ISSN:1529-2401, 1529-2401
On-line prístup:Zistit podrobnosti o prístupe
Tagy: Pridať tag
Žiadne tagy, Buďte prvý, kto otaguje tento záznam!
Popis
Shrnutí:Dyskinesia represents a debilitating complication of L-3,4-dihydroxyphenylalanine (L-dopa) therapy for Parkinson's disease. Such motor manifestations are attributed to pathological activity in the motor parts of basal ganglia. However, because consistent funneling of information takes place between the sensorimotor, limbic, and associative basal ganglia domains, we hypothesized that nonmotor domains play a role in these manifestations. Here we report the changes in 2-deoxyglucose (2-DG) accumulation in the sensorimotor, limbic, and associative domains of basal ganglia and thalamic nuclei of four groups of nonhuman primates: normal, parkinsonian, parkinsonian chronically treated with L-dopa without exhibiting dyskinesia, and parkinsonian chronically treated with L-dopa and exhibiting overt dyskinesia. Although nondyskinetic animals display a rather normalized metabolic activity, dyskinetic animals are distinguished by significant changes in 2-DG accumulation in limbic- and associative-related structures and not simply in sensorimotor-related ones, suggesting that dyskinesia is linked to a pathological processing of limbic and cognitive information. We propose that these metabolic changes reflect the underlying neural mechanisms of not simply motor dyskinesias but also affective, motivational, and cognitive disorders associated with long-term exposure to L-dopa.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1529-2401
1529-2401
DOI:10.1523/JNEUROSCI.5059-04.2005