[Mechanisms of regulating monoamine oxidase activity in different brain regions].

Both in vitro and in vivo rates of oxidative deamination of 3H-dopamine (DA), 14C-tyramine (T), 14C-noradrenaline (NA), 3H-serotonine (S) and benzylamine (BA) by monoamine oxidases of homogenates of rat brain cortex, brain stem and basal ganglia were shown to be different either after administration of l-dihydroxyphenylalanine (l-DOPA) and of N1-d,l-seryl-N2/(2,3,4-trihydroxybenzyl) hydrazine (Ro 4-4602) or after their simultaneous administration into the animals. L-DOPA and Ro 4-4602, administered intraperitoneally at a dose of 50 mg/kg, did not affect distinctly the NA and S deamination in various parts of brain. Ro 4-4602 inhibited selectively the BA deamination in basal ganglia; simultaneous administration of the drug together with l-DOPA caused more pronounced inhibition of BA deamination; it decreased also the rate of deamination of DA and T in the ganglia. L-DOPA, Ro 4-4602 and their combination were especially effective at concentration 10(-4) M. These data characterize one of possible mechanisms of distinct antiparkinsonic action of these drugs. Ro 4-4602 was shown to inhibit the deamination of DA and S noncompetitively. L-DOPA (10(-5)--10(-4) M) activated selectively the DA deamination in brain mitochondria.