ISSN:
1435-1463
Keywords:
[14C]-2DG uptake
;
MPTP
;
marmoset
;
basal ganglia
;
behavioural recovery
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary The “short-term” (0.7 ± 0.1 months post-MPTP) and “long-term” effects (36.7 ± 4.4 months) of MPTP treatment on motor behaviour and [14C]-2DG uptake were investigated in the common marmoset. The subcutaneous administration of MPTP greatly reduced locomotor activity (−94% with respect to controls) and induced motor disability in the “short-term” MPTP-treated marmoset group. In the “long-term” MPTP group, MPTP treatment did not significantly affect locomotor activity (−27% with respect to controls) and there was partial recovery of motor disability. In the “short-term” MPTP group, there were increases in [14C]-2DG uptake in the GP1 (+31 to +37%), SNc (+34 to +42%), VTA (+35%), LC (+23%), PPN (+19%) and in the VA (+19%), VL (+20%) and AM (+17%) thalamic nuclei. [14C]-2DG uptake was decreased in the STN (−15%). In the “long-term” MPTP group, [14C]-2DG uptake was increased in the GP1 (+18%), SNc (+27%), VTA (+25%), PPN (+19%), ventral caudate nucleus (+18 to +23%), NAc (+22%), F.Ctx (+18%) and in the VA (+34%), VL (+28%), AV (+33%) and AM (+24%) thalamic nuclei. [14C]-2DG uptake was unchanged in the STN. The increase in metabolic activity of the surviving DA neurones and/or the reactive gliosis may account for the initial increase in [14C]-2DG uptake in the SNc and VTA. On the other hand, in the “long-term” MPTP-treated animals the increase in [14C]-2DG uptake in the SNc (though less than in the “short-term” MPTP group), ventral caudate and NAc may reflect the regenerative changes in the dopaminergic system in these areas. Despite the behavioural recovery, [14C]-2DG uptake remained elevated in the target areas for medial paludal output (the thalamic nuclei and PPN). However, the attenuation of the changes in [14C]-2DG uptake in the GP1 and STN of “longterm” MPTP-treated marmosets suggest that the striato-GPl and GP1-STN outputs closely reflect motor function in this primate model of Parkinson's disease.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF01271546
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