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development of IAA was thought to be very likely as a result of oxidase deamination of NMT (Barker et al., 1980), but was later recognized to generally be also in part by immediate deamination by MAO (Barker et al., 1982). Pretreatment Along with the MAO-I iproniazid in rat entire brain homogenates inhibited IAA development by eighty three%, NMT an