Serotonin, Alcohol, SSRI and Tianeptine: What is the Interaction?

Overview

Pharmacological effects of alcohol may help in understanding the consequence of the differencein the mechanism of action of antidepressants inhibiting the reuptake of monoamines (RUI) andtianeptine which increases serotonin reuptake.Alcohol, similarly as reserpine, increases serotonin release into the synaptic cleft followed by itsfast enzymatic metabolization. A long-term high consumption of alcohol may cause chronic defi citof serotonin and „pharmacogenic“ depression which is worsened by chronic stress induced by socialand economic degradation of the alcoholic.RUI increase the concentration of serotonin in the synaptic cleft, but serotonin does not decreasethe activation of the hypothalamo-pituitary-adrenal axis. Antidepressant effects of RUI can beexplained by the events beyond the synaptic receptors, esp. by an amelioration of neuroplasticityand a correction of structural defi cits in hippocampus and other brain areas.Tianeptine does not increase the concentration of serotonin in the synaptic cleft and keeps it fromenzymatic degradation. Tianeptine shields hippocampus from the noxious effects of stress ondendrites. On this level, its effects are comparable to the effects of RUI.Favourable therapeutic effects of some RUI in alcohol dependence are connected probably withthe fi rst step of their action, i.e. increase of concentration of serotonin in the synaptic cleft whichsimulates the acute action of alcohol. The missing evidence of therapeutic effects of tianeptinein nondepressed alcoholics might be explained by the fact that it does not increase serotoninconcentration in the synaptic cleft.On the other hand, the increase of serotonin reuptake by tianeptine might have an advantage overserotonin reuptake inhibition in the treatment of depression in patients dependent on alcohol,because it has a more direct protective effects from stress.

Key words:
alcohol, serotonin, depression, SSRI, tianeptine.