The catecholamine theory suggests that there is a functional deficit of the catecholamine neurotransmitter, norepinephrine (NE) or dopamine (DA) at the neuronal synaptic cleft in depression and an excess in mania. Current strategies which are being utilized to investigate this theory involve: 1)studies of DA, NE, their breakdown products and synthetic and degradative enzymes in body fluids and brain tissue; 2) studies of modes of action of drug which can "activate" or decrease manic or depressive symptoms; 3) the study of pharmacological agents which affect specific aspects of NE and DA metabolism, (synthesis, release, receptor sensitivity, and degradation). The total accumlated data seems more compatible with a catecholamine hypothesis of mania than one of depression. The evidence to date does not allow one to differentiate between the importance of DA or NE either in depression of mania.