Involvement of sensorimotor, limbic, and associative basal ganglia domains in L-3,4-dihydroxyphenylalanine-induced dyskinesia
Journal of Neuroscience. 2005-02-23; 25(8): 2102-2107
DOI: 10.1523/JNEUROSCI.5059-04.2005
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1. J Neurosci. 2005 Feb 23;25(8):2102-7.
Involvement of sensorimotor, limbic, and associative basal ganglia domains in
L-3,4-dihydroxyphenylalanine-induced dyskinesia.
Guigoni C(1), Li Q, Aubert I, Dovero S, Bioulac BH, Bloch B, Crossman AR, Gross
CE, Bezard E.
Author information:
(1)Basal Gang, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de
Recherche (UMR) 5543, Université Victor Segalen-Bordeaux 2, 33076 Bordeaux Cedex,
France.
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.
DOI: 10.1523/JNEUROSCI.5059-04.2005
PMID: 15728850 [Indexed for MEDLINE]