DHNB

3,4-Dihydroxy-5-fluorophenylalanine, fluorodopa, was injected into rats in which unilateral lesions of the nigrostriatal pathway had been made. The rats rotated towards the side with the lesions, thus providing further evidence that fluoro-dopa is an analogue of dopa. [ 18 F]Fluoro-dopa was then injected intravenously into fully conscious baboons. A well-collimated scintillation detector, aligned along the occipitomental axis, recorded the accumulation of 18 F in the brain. Control animals accumulated 18 F continuously for 100 min. This accumulation represents net transport of [ 18 F]fluoro-dopa from blood to brain, decarboxylation to [ 18 F]fluoro-dopamine, storage, and degradation of [ 18 F]fluoro-dopamine. α-Methyl-dopa, a competitive inhibitor of dopa transport and decarboxylation, prevented the accumulation of 18 F; reserpine, known to release stored intracerebral dopamine, discharged 18 F; pargyline, a monoamine oxidase inhibitor, and haloperidol, a known augmentor of intracerebral dopamine turnover, increased the rate of accumulation of 18 F. These changes in the accumulation of intracerebral 18 F, after [ 18 F]fluoro-dopa, were commensurate with the known action of the drugs used to induce them and demonstrate the use of a γ-emitting precursor of a neurotransmitter to monitor simply, atraumatically, and externally the intracerebral metabolism of the transmitter in fully conscious primates. When applied to man, the same technique should be able to provide more conclusive evidence than is presently available for the role of catecholamines in schizophrenia and depression. It should also provide further insight into the natural history of nigrostriatal diseases and the action of drugs used in their treatment.