Monoaminoxydase-Hemmer

Effect of caroxazone, a new antidepressant drug, on monoamine oxidases in healthy volunteers.

“…Although the increase in tryptamine urinary excretion reflects MAO inhibition in the whole body, it is conceivable that it could also take place in brain where tryptamine is usually absent and accumulates after treatment with MAOIs. Moreover, it has been repeatedly shown in rats that the level of other monamines in brain is also increased by caroxazone administration (Moretti et al, in preparation; Ponzio, Curcio, Brunello & Algeri, personal communication), as well as by all other MAOIs tested in animals (Green & Youdim, 1975;Maitre, DeliniStula & Waldmeier 1976;Pletscher, Gey & Zeller, 1960;Sharman, 1976;Valzelli & Garattini, 1968;Yang & Neff, 1974) and in man (Bevan Jones, Parte, Nicholson, Price & Stacey, 1972;Maclean, Nicholson, Pare & Stacey, 1965). However there is a difference between caroxazone and all other clinically-used MAOIs, namely the apparent lack of effect on platelet MAO.…”

Influence of Iproniazid on Norepinephrine Content in Gastric Wall Tissue under Experimental Dystrophy

“…Such an injection, as shown in our previous work, protects the gastric wall from Zavodskaya and Zabrodin, Influence of Iproniazid dystrophy [17]. These effects may be explained by the property of iproniazid to retain catecholamines in the storing granules, preventing their output and their following depletion under the influence of reserpine or of nervous stimulation [5,10,13].…”

“…Evidence of I lie probable role of catecholamine depletion for development of dystrophy are the results which show that high doses of reserpine, which cause such depletion of catecholamine stores in tissues and organs of rats [5,7,13], lead to gastric wall ulcerations [6,11,19].…”

Review of the pharmacology of existing antidepressants.

“…It follows that inhibition of MAO is accompanied by an increase in tissue levels ofall three amines. It is believed that antidepressant activity results from the spontaneous spilling over of these amines into the neuronal synapse, but it can also be argued that more amines are available for release by specific neuronal activity, particularly if previously amine synthesis and/ or storage was impaired (for reviews, see Pletscher et al, 1960;Pletscher, 1968;Costa & Sandler, 1972).…”