Opiate receptor avidity is reduced in non-motor impaired MPTP-lesioned rhesus monkeys

Opiate receptor avidity, roughly equivalent to the ratio of unoccupied receptor density to the receptor dissociation constant ( B′ max/ K D), was measured in four MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-lesioned rhesus monkeys and nine normal controls with positron emission tomography (PET) and 6-deoxy-6-β-[ 18 F ]fluoronaltrexone (cyclofoxy, CF), a μ- and κ-opiate receptor antagonist. Although the MPTP-lesioned monkeys were dopamine deficient as measured with [ 18 F ]- l-fluorodopa ([ 18 F ]-DOPA) and PET [Doudet et al., 6-[ 18 F ]- l-DOPA imaging of the dopamine neostriatal system in normal and clinically normal-MPTP-treated rhesus monkeys, Exp. Brain Res. 78 (1989) 69–80], they had clinically recovered from the acute motor effects of MPTP exposure. Opiate receptor avidity was found to be reduced by 30–35% in the opiate-receptor rich areas of caudate, anterior putamen, thalamus, and amygdala of the MPTP-lesioned animals. The results suggest that opiate pathways make a significant contribution to the adjustment of cortico–striatal–thalamic pathway activity and thereby to behavior in rhesus monkeys following dopamine loss.