The employment of drugs acting on the central nervous system has been predicated largely on an empirical basis, the anticholinesterase compounds serving as an exception. As our understanding of the chemical constituents and their function in brain broadens, one can begin to see that basic theoretical information will be the foundation for new therapeutic approaches in this field. The observation that the effect of reserpine may be mediated through its action on liberating serotonin,2 the changes observed with diethylaminoethanol, an analogue of acetylcholine,3 and the utilization of antimetabolites of serotonin,4 all of which modify behavior, are a few examples of this theoretical approach.
It has been found that iproniazid is a potent monoamine oxidase inhibitor in vivo,5 and since serotonin can be degraded by this enzyme, it is apparent that the mechanism of action of such a drug may result in an increase in cerebral serotonin,
LAUER JW, INSKIP WM, BERNSOHN J, ZELLER EA. Observations on Schizophrenic Patients After Iproniazid and Tryptophan. AMA Arch NeurPsych. 1958;80(1):122–130. doi:10.1001/archneurpsyc.1958.02340070140021
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