PHARMACOLOGICAL MODIFICATIONS OF DOPAMINE TRANSMISSION DO NOT INFLUENCE THE STRIATAL IN-VIVO BINDING OF [H-3] MAZINDOL OR [H-3] COCAINE IN MICE

We have considered the in vivo striatal binding of two ligands of the neuronal dopamine uptake complex: [H-3]cocaine and [H-3]mazindol. The [H-3]cocaine tracer dose labelled the dopamine uptake complex in stria tum but not the noradrenaline complex in cerebellum. On the contrary, the [H-3]mazindol tracer dose induced a marked labelling of the noradr enaline uptake complex in cerebellum; its prevention by desipramine (5 mg/kg) increased simultaneously the cerebral bioavailability and ther eby the striatal labelling of the dopamine transporter. In mice submit ted to treatments modifying dopaminergic transmission either to decrea se it (gammabutyrolactone, 750 mg/kg, i.p.) or to increase it (L-DOPA, 200 mg/kg, i.p., dexamphetamine, 4 mg/kg, s.c., or their combination) , only dexamphetamine pretreatment significantly reduced [H-3]cocaine and [H-3]mazindol binding. Thus it appears that the level of dopamine transmission would not interfere with the in vivo quantification of st riatal dopamine uptake sites assessed with either ligands.