[Interrelations between neuromediators implicated in depression and antidepressive drugs]

The concept that specific neurons modulate information processing rather than they convey sensory or motor signals seems to be well established. In any representation of the primary pathways responsible for the processing of sensory stimuli or motor outputs, it is notable that noradrenergic, serotonergic or dopaminergic neurons do not appear to be involved. Noradrenergic and serotonergic cells are activated by non specific stimuli coming from all sensory modalities, whereas dopaminergic neurons are activated by stimuli related to motivation, and which have previously taken a significance over the animal's history. Dopaminergic neurons activation therefore depends upon cortical processings which necessitate the participation of noradrenergic and serotonergic neurons. Up to now the clinical efficacy of antidepressants has been correlated with their biochemical property to desensitize cortical beta 1-adrenergic receptors. This does not necessarily mean that this desensitization is essential, but rather that these receptors are extremely sensitive to modifications of noradrenergic transmission and that a reactivation of noradrenergic transmission is central for depression relief. Taking into account data from the literature and results obtained in our laboratory, we propose: 1) that the reactivation of serotonergic neurons is essential to reactivate noradrenergic cells; 2) that the presence of a normal noradrenergic transmission is necessary to obtain a functional subcortical dopaminergic transmission.(ABSTRACT TRUNCATED AT 250 WORDS)