Dopamine depleting lesions of the substantia nigra result in a reduction of the striatal accumulation of 2-phenylethylamine following monoamine oxidase inhibition. It is established that this effect may not be due to a change in availability of aromaticL-amino acid decarboxylase in striatum. Nevertheless, the possibility remains that striatal concentrations of phenylalanine (the precursor of 2-phenylethylamine) may be altered by dopamine-depleting lesions. The present experiments assessed the effects of dopamine depletion induced by 6-OHDA (7 days following 8 μg/4 μl unilateral substantia nigra injection) on striatal concentrations of phenylalanine, dopamine, 5-hydroxytryptamine and their metabolites. In addition, the effects of reserpine-induced (10 mg kg−1, 2h, sc) amine depletion on these striatal levels were also assessed. Under equivalent conditions reserpine is reported to increase striatal accumulationof 2-phenylethylamine. 6-OHDA induced a significant unilateral depletion of dopamine, DOPAC and HVA and increased 5-HIAA but had no significant effect on phenylalanine levels. Reserpine decreased dopamine and 5-hydroxytryptamine and increased DOPAC, HVA and 5-HIAA levels, no changes in phenylalanine were observed. This pattern of results was also observed when lesioned animals or reserpine-treated animals were pretreated with (-)-deprenyl (2 mg kg−1, 2 hr, sc), the treatment previously used to induce accumulation of 2-phenylethylamine. These data indicate that changes in 2-phenylethylamine previously observed under these conditions may not simply be secondary to a change in striatal phenylalanine concentra
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