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The effects of oral oxprenolol (480 mg) and lorazepam (2 mg) on skin conductance, reaction time, critical flicker frequency and self-rating visual analogue scales for anxiety, sedation and concentration were investigated in 6 healthy male volunteers. Oxprenolol exerted a central action similar to lorazepam as shown by a significant lowering of skin conductance and decrease in the number of spontaneous fluctuations during stress, impaired critical flicker frequency and decrease in alertness with reduced concentration.

The selective monoamine oxidase (MAO) B inhibitor (-)deprenyl failed to produce any greater benefit than placebo in a limited double-blind trial conducted in depressive patients. Its relative freedom from the so-called cheese effect was confirmed, however, in drug-treated patients challenged IV with tyramine. There is evidence to suggest that this cheese effect, a facilitated tyramine-induced hypertensive response, is pharmacologically distinct from MAO inhibition proper. Thus, it is conceivable that its central counterpart, an enhanced noradrenaline release due to the access of traces of tyramine to the CNS, is a prerequisite for any therapeutic benifit obtainable with the MAO-inhibitory drugs in general.

The effects of protriptyline and clomipramine, at concentrations of 10-7 M to 10-4 M, were studied in vitro on the uptake of 5-hydroxytryptamine and dopamine uptake in human platelet-rich plasma. It was found that the tertiary amine, clomipramine, was a more potent inhibitor of 5-hydroxytryptamine uptake than the secondary amine, protriptyline. The activity of both compounds was competitive but it was thought unlikely that they acted through tryptamine receptor sites as methysergide 2.5×10-8 M had very little effect on 5-hydroxytryptamine uptake. Neither tricyclic antidepressant had any marked effect on dopamine uptake.

IT is well recognized that monoamine oxidase (monoamine: O2oxidoreductase (deaminating), EC 1.4.3.4) (MAO) plays an important role in the degradation of biologically active monoamines in the brain1,2. There is much evidence pointing to changes in monoamine metabolism in mental illnesses characterized by alterations in mood3,4. Perhaps the most important property of MAO inhibiting drugs is their ability to bring about a lightening of affect in depressed patients5. That this effect results solely from the inhibition of MAO has not been widely questioned, although the antidepressive effect is not shared to an equal extent by all drugs in the group6. An attempt has been made to explain this finding in terms of differing ability of the MAO inhibitors to prevent amine re-uptake7; however, it has seemed to us that an explanation might better be sought in terms of differential inhibitory capacity of these drugs on the four molecular variants of MAO in the human brain8.