Competition between 11C-raclopride and endogenous dopamine in Parkinson's disease

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.

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.

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.

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.