The new molecular targets for antidepressants

The efficacy of depressive disorders treatment is insufficient. It is explained by an incomplete understanding of both pathogenesis of depression and antidepressants mechanism action. An improvement of the treatment efficacy of depression disorders is closely associated with complete knowledge of the pathogenesis of disorders and antidepressant mechanism of action. The effect produced by the first line of antidepressants prescribed currently in the clinical practice includes the accumulation of monoamines and prolonged activation of their membrane receptors. However, a decrease in the membrane receptors density evoked by prolonged activation of monoaminergic receptors is counteracted by the second line of antidepressant activity. It is associated with the expression of inducible regulatory protein S100A10 (p11) and its partners. In this review, the authors examined the structure and function of protein p11, its interaction with such proteins as annexin A2, Ahnak, chromatinremodeling factor SMARCA3. The authors analyzed the influence of p11 on the membrane density of serotonin 5-HT1B and 5-HT4 receptors, metabotropic glutamate receptors 5, voltage-dependent potassium Kv3, and calcium Cav1.2 and 1.3 channels, that play an important role in both the effect of antidepressants and the pathogenesis of depression disorders. A systematic literature search was conducted in Scopus, Web of Science, MedLine, elibrary, and other databases.