Neural mechanisms underlying parkinsonian symptoms based upon regional uptake of 2-deoxyglucose in monkeys exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine

Mitchell, Ian; Clarke, Carl E; Boyce, S.; Robertson, R. G. H.; Peggs, David; Sambrook, M.A.; Crossman, Alan R.

doi:10.1016/0306-4522(89)90120-6

Cited by 439 publications

(220 citation statements)

References 41 publications

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“…The pattern of changes in 2-DG accumulation in our experimental groups matches the original findings of Mitchell et al (1989Mitchell et al ( , 1992. For instance, we do confirm the differential metabolic activity between the motor component of the STN, the dorsolateral tip, and the ventromedial limbic-associative STN in both nondyskinetic and dyskinetic animals.…”

Section: Discussionsupporting

confidence: 91%

“…1, Table 2). No significant change was observed in 2-DG uptake in the SNr (F (3,17) ϭ 3.61; p Ͻ 0.05) in any group, as reported previously (Mitchell et al, 1989(Mitchell et al, , 1992Bezard et al, 2001a).…”

Section: Methodssupporting

confidence: 86%

“…On the day they were killed, animals were given an intravenous injection of 1 mCi/kg [ 3 H]2-DG (specific activity, 50 Ci/ mmol, 185 GBq/mmol; Interchim, Grenoble, France) in sterile saline as described previously (Mitchell et al, 1989;Bezard et al, 2001a). After 45 min, all animals were killed by sodium pentobarbital overdose (150 mg/ kg, i.v.).…”

Section: Methodsmentioning

confidence: 99%

“…Interestingly, Mitchell et al showed in their 2-deoxyglucose (2-DG) seminal studies (Mitchell et al, 1989(Mitchell et al, , 1992) that the motor component of the subthalamic nucleus (STN), the dorsolateral tip, had normal terminal activity in chorea that was increased significantly in dystonia, whereas the metabolic activity of the ventromedial "limbic/associative" STN was impaired in both cases. This result originally suggested pathophysiological differences between L-dopa-induced chorea and dystonia.…”

Section: Introductionmentioning

confidence: 99%

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Involvement of Sensorimotor, Limbic, and Associative Basal Ganglia Domains in L-3,4-Dihydroxyphenylalanine-Induced Dyskinesia

Guigoni

Li²,

Aubert³

et al. 2005

J. Neurosci.

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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 sensorimotorrelated 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.

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Section: Discussionsupporting

confidence: 91%

Section: Methodssupporting

confidence: 86%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Involvement of Sensorimotor, Limbic, and Associative Basal Ganglia Domains in L-3,4-Dihydroxyphenylalanine-Induced Dyskinesia

Guigoni

Li²,

Aubert³

et al. 2005

J. Neurosci.

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“…Choice of the STN as a target for PD arose from studies on the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkey model of PD, which showed increased neuronal activity in the STN [13] and marked amelioration of parkinsonian features following its lesion [14]. This antiparkinsonian effect could be reproduced with DBS of the STN in this model [15] and later in PD patients [16,17].…”

Section: Introductionmentioning

confidence: 99%

Deep brain stimulation: from neurology to psychiatry?

Krack

Hariz

Baunez

et al. 2010

Trends in Neurosciences

271

186

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International audienceFunctional stereotaxy was introduced in the late 1940s to reduce the morbidity of lobotomy in psychiatric disease by using more focal lesions. The advent of neuroleptics led to a drastic decline in psychosurgery for several decades. Functional stereotactic neurosurgery has recently been revitalized, starting with treatment of Parkinson's disease, in which deep brain stimulation (DBS) facilitates reversible focal neuromodulation of altered basal ganglia circuits. DBS is now being extended to treatment of neuropsychiatric conditions such as Gilles de la Tourette syndrome, obsessive-compulsive disorder, depression and addiction. In this review, we discuss the concept that dysfunction of motor, limbic and associative cortico-basal ganglia-thalamocortical loops underlies these various disorders, which might now be amenable to DBS treatment

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