Dysbalance of neuronal second messenger function in the aetiology of affective disorders: a pathophysiological concept hypothesising defects beyond first messenger receptors.

It is suggested that affective disorders arise from the dysbalance of the two major intraneuronal signal amplification systems, the adenylate cyclase and the phospholipase C system, with depression resulting from underfunction of cyclic adenosine 3',5'-monophosphate-mediated effector cell responses associated with an absolute or relative dominance of the inositoltriphosphate/diacylglycerol-mediated responses and mania resulting from the converse. The usefulness of this hypothesis is discussed with respect to (a) the mechanism of action of current therapeutic agents and (b) the development of novel therapeutic approaches.