["Atypical" antidepressive mechanisms: glutamatergic modulation and neuroplasticity in case of tianeptine].

Recent neurobiological and clinical studies demonstrated that neuroplasticity, a principal mechanism of neuronal adaptation and survival, was disrupted in major depression and in long-term stress. Increasing research data show, that structural remodeling and maladaptive dysfunction of certain brain regions is a main component of major depressive illness. Tianeptine, an "atypical" antidepressant, which has a pharmacological action different from the "typical" reuptake blocking agents, underlined a re-evaluation of the neurobiological basis of major depression and revealed that the disorder cannot be explained only by the classic monoamine hypothesis. Neuroplasticity hypothesis of major depression brings the possibility to make important contributions to the diagnosis, however, it may helpful in the understanding the detailed subtle drug effects, which cannot be revealed by pure neurochemical mechanisms. In this review, effects of tianeptine on neuroplasticity, neuroprotection, neurogenesis, hippocampal stress response, long term potentiation, and, as well as on the glutamatergic system and other neuronal networks are evaluated.