Clinical originality and new biology of trimipramine.
Trimipramine differs from other antidepressant drugs in a number of ways. Although trimipramine shares equivalent efficacy with doxepin, imipramine, maprotiline and amitriptyline, as evidenced by double-blind studies, it possesses a different side-effect profile. Trimipramine is considered to be less cardiotoxic, and data presented in this paper support its minimal effect on orthostatic hypotension, as compared with clomipramine. In addition, trimipramine has less epileptogenic potential than other antidepressants such as imipramine, amitriptyline and maprotiline. Besides this different side-effect profile, trimipramine exerts differing effects on neurotransmitter functions and their reuptake. For example, trimipramine does not inhibit reuptake of noradrenaline and serotonin, and does not down-regulate beta 1-adrenoceptors. Furthermore, in common with lithium, trimipramine produces enhancement of antidepressant action in treatment-resistant depressed patients. There is evidence that trimipramine enhances the sensitivity of cortical neurons to noradrenaline after prolonged administration and may also increase the activity of serotonin neurons.
Gastpar
M
M
Klinik für allgemeine Psychiatrie, Rheinische Landes- und Hochschulklinik, Essen, Federal Republic of Germany.
D003866:Depressive Disorder / Q000188:drug therapy* / Q000523:psychology; D003984:Dibenzazepines / Q000627:therapeutic use*; D006801:Humans; D011954:Receptors, Dopamine / Q000187:drug effects; D012890:Sleep / Q000187:drug effects; D014299:Trimipramine / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*
D003984:Dibenzazepines; D011954:Receptors, Dopamine; D014299:Trimipramine