Résumé
The common mechanism of action of most tricyclic antidepressants is the inhibition of the reuptake of the biogenic amines norepinephrine, serotonin and dopamine. Another postulated mechanism of action for most is the down-regulation of beta-adrenergic receptors post-synaptically and [alpha]2 heteroreceptors on 5-HT terminals. Other produce down-regulation of 5-HT1and 5-HT2 receptors. Neither of these mechanisms fully account for a common antidepressant mechanism of action. Is it possible to unify these hypotheses of antidepressant action = A number of receptor changes have been recognized in depression. Usually, those receptors are linked to a G protein. Thus, it could be hypothesized that depression may be the result of a disorder of the large family or receptor-linked G proteins. This genetically-determined disorder could be expressed in either the receptor or in the G proteins leading to a defective linkage between the receptor and the G protein resulting in abnormal transduction mechanisms. The concept of antidepressants is changing rapidly as these agents appear with new therapeutic indications other than depression such as panic disorder obsessive-compulsive disorder, etc. it can be expected that the presently available antidepressants might eventually be considered as anxiolytics or that benzodiazepines [5-HT1A agonists] could come to be viewed disinhibiting substances