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Journal of Pharmacology And Experimental Therapeutics, Vol. 128, Issue 1, 15-21, 1960
Copyright © 1960 by American Society for Pharmacology and Experimental Therapeutics

BIOCHEMICAL AND PHARMACOLOGICAL EFFECTS OF THE MONOAMINE OXIDASE INHIBITORS, IPRONIAZID, 1-PHENYL-2-HYDRAZINOPROPANE (JB 516) AND 1-PHENYL-3-HYDRAZINOBUTANE (JB 835)

Sydney Spector 1, Parkhurst A. Shore 1, and Bernard B. Brodie 1

1 Laboratory of Chemical Pharmacology, National Heart Institute, National Institutes of Health, Bethesda, Maryland

Iproniazid and two phenylalkylhydrazines, 1-phenyl-2-hydrazinopropane (JB 516) and 1-phenyl-3-hydrazinobutane (JB 835), administered to rabbits in repeated doses, cause a rapid elevation in brain serotonin and a slower rise in brain norepinephrine. Central excitation is temporally related to the rise in brain norepinephrine but not to the blocking of MAO or to the elevation of brain serotonin. The elevation of norepinephrine suggests that MAO is portant for the in vivo metabolism of brain norepinephrine, at least in rabbit and rat.

The three MAO inhibitors act differently in various species. Thus they elevate the brain levels of serotonin but not of norepinephrine in dogs and cats, and do not elicit the pronounced central excitation in these species. Serotonin levels in dogs are elevated about 7-fold over a period of 3 weeks of daily drug administration.

The rapid disappearance of MAO blockade in the mouse suggests that the enzyme may be rapidly formed in this species compared to the rabbit

A view is presented that an important function of MAO in brain may be to control the amounts of biogenic amines in the neuron.

Submitted on July 15, 1959




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J. J. Schildkraut and S. S. Kety
Biogenic Amines and Emotion
Science, April 7, 1967; 156(3771): 21 - 30.
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