The effects of the peripheral aromatic amino acid decarboxylase (AADC) 
inhibitors, carbidopa and benserazide, and the central AADC inhibitor, 
3-hydroxybenzylhydrazine (NSD-1015) on peripheral and brain monoamine oxidase 
(MAO) A and B activity were investigated in the rat. In vitro, carbidopa, 
benserazide and NSD-1015 all potently inhibited hepatic MAO A and B activity 
(IC(50) 10-50 micro M). In ex vivo studies following systemic drug 
administration, NSD-1015 (100 mg/kg ip) produced 88% and 96% inhibition of 
hepatic and striatal MAO A and B activity respectively. Carbidopa (12.5 mg/kg 
i.p.) and benserazide (50 mg/kg i.p.) had no effect on striatal MAO A activity 
or hepatic MAO B activity. However, they inhibited striatal MAO B activity by 45 
+/- 10% and 36 +/- 10% respectively. In conclusion, carbidopa and benserazide 
may not only protect L-DOPA from peripheral decarboxylation, but also increase 
striatal dopamine content through MAO inhibition. NSD-1015 should not be used to 
investigate the neuromodulatory role of L-DOPA as it potently inhibits rat 
striatal MAO.