1. (-)-Deprenyl has been shown to potentiate rat striatal neurone responses to 
dopamine agonists at doses not altering dopamine metabolism. Since there are a 
number of effects of (-)-deprenyl which could result in this phenomenon, we have 
investigated the effects of MDL 72,145 and Ro 19-6327, whose only common effect 
with (-)-deprenyl is an inhibition of monoamine oxidase-B (MAO-B), on rat 
striatal neurone responses to dopamine and on striatal dopamine metabolism. 2. 
Using in vivo electrophysiology, i.p. injection of either MDL 72,145 or Ro 
19-6327 was found to produce a dose-dependent potentiation of striatal neurone 
responses to dopamine but not gamma-aminobutyric acid. 3. Neurochemical 
investigations revealed that this occurred at doses (0.25-1 mg kg-1) which, 
while not affecting levels of dopamine or its metabolites, 
3,4-dihydroxyphenylacetic acid or homovanillic acid, did cause a significant, 
dose-dependent, elevation in striatal levels of the putative neuromodulator, 
2-phenylethylamine (PE). 4. Inhibition of PE synthesis by i.p. injection of the 
aromatic L-amino acid decarboxylase inhibitor, NSD 1015, produced a reversal of 
the effects of MDL 72,145 and Ro 19-6327. 5. Neurochemical analysis revealed 
this to occur at a dose of NSD 1015 (10 mg kg-1) selective for reduction of 
elevated PE levels. 6. These results suggest that PE can act as a neuromodulator 
of dopaminergic responses and that MAO-B inhibitors may potentiate neuronal 
responses to dopamine via the indirect mechanism of elevation of PE following 
MAO-B inhibition.