Objective: The aim of this study was to understand whether the increase in 11C-raclopride binding in the striatum of patients with Parkinson's disease (PD) is associated with the depletion of endogenous dopamine.
Methods: Positron emission tomography (PET) scans of the two dopamine D2 receptor ligands, 11C-raclopride and 11C-N-methylspiperone (11C-NMSP), and the dopamine transporter ligand, 11C-2beta-carbomethoxy-3beta-(4-fluorophenyl)-tropane, were performed on five patients with PD and seven controls. The binding of each tracer was calculated by using a (region-cerebellum)/cerebellum ratio in the caudate, anterior putamen, and posterior putamen.
Results: In patients with PD, the 11C-raclopride to 11C-NMSP ratios in the posterior putamen, which was the subregion of the striatum with the lowest binding of 11C-2beta-carbomethoxy-3beta-(4-fluorophenyl)-tropane, were the largest among all three subregions of the striatum. In controls, the 11C-raclopride to 11C-NMSP ratios in all three subregions of the striatum were within a constant range.
Conclusion: In patients with PD, the kinetic difference between 11C-raclopride and 11C-NMSP was found prominently in the posterior putamen, in which presynaptic degeneration occurred most profoundly. Therefore, we concluded that the increase in 11C-raclopride binding in the striatum of patients with PD was strongly associated with the depletion of endogenous dopamine. 11C-NMSP can be chosen in the place of 11C-raclopride in cases in which it may be essential to eliminate the influence of endogenous dopamine.