Resent research on the mechanisms of action of antidepressant treatmen
t (ADT) has led to major revision of earlier concepts. The monoamine d
eficiency hypothesis seems to be too simplistic, as it does not accoun
t for the great temporal discrepancy between the rapid drug-induced bi
ochemical effects of amine uptake and catabolism, which occurs within
hours, and the antidepressant response, which occurs after at least 7-
14 days. The pharmacodynamic effects of ADT are obviously complex invo
lving a great number of interacting transmitter and receptor systems i
n the central nervous system. Secondary adaptive changes in neuronal s
ystems seem to play an integral and possibly pivotal role in antidepre
ssant drug action. Our knowledge about the details is sparse, primaril
y because most investigations on the subject are based on animal studi
es or in vitro technics, whereas the number of clinical investigations
of the antidepressant drug effect on the living human organism is lim
ited. This fact may explain the often-found discrepancy between experi
mental and clinical effect.