SHORT AND LONG-TERM CHANGES IN CEREBRAL [C-14] 2-DEOXYGLUCOSE UPTAKE IN THE MPTP-TREATED MARMOSET - RELATIONSHIP TO LOCOMOTOR-ACTIVITY

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 [C-14]-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 [C-14]-2DG uptake in the GPl (+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. [C-14]-2DG uptake was decreased in the STN (-15%). In the ''long-term'' MPTP group, [C-14]-2DG uptake was increased in the GPl (+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. [C-14]-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 [C-14]-2DG uptake in the SNc and VTA. On the other hand, in the ''long-term'' MPTP-treated animals the increase in [C-14]-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, [C-14]-2DG uptake remained elevated in the target areas for medial pallidal output (the thalamic nuclei and PPN). However, the attenuation of the changes in [C-14]-2DG uptake in the GPI and STN of ''long-term'' MPTP-treated marmosets suggest that the striato-GPl and GPl-STN outputs closely reflect motor function in this primate model of Parkinson's disease.