50 patients with depression who had been considered suitable for E.C.T. were given iproniazid in doses up to 450 mg/day for periods varying from two to forty weeks.

MItochondrial fractions were isolated from bovine tissue homogenates of bovine brain and suspended in 0.1 M phosphate buffer (pH 7.4). Mitochondrial fractions were pre-incubated with 5-HT (1 mM), 2-phenylethylamine (0.8 mM), tyramine (3.2 mM), dopamine (3 mM) or Hi (10 mM) at 37 deg-C for 30 - 45 minutes. Bovine mitochondrial were further incubated with increasing concentrations of Iproniazid (0.001 to 0.1 mM) which caused gradual inhibition of the deamination of 5-HT, tyramine, and dopamine. At 1 mM of Iproniazid, there was a marked increase in HDA, which was quite small in the mitochondria not treated with Iproniazid. Treatment of bovine brain mitochondria with 1 mM Iproniazid did not induce the appearance of HDA if the catalytic sites of the MAO-A were blocked by clorgyline. A selective inhibitor of the MAO-B deprenyl did not prevent the appearance of HDA after treatment with Iproniazid.