ABSTRACT
The pharmacotherapeutic approach to affective disorders, from the perspective of current scienti˜c pharmacology, has its origin in the 1950s, the same decade in which the ˜rst antipsychotic and anxiolytic agents appeared, and what has been termed the “revolution of psychopharmacology” (López-Muñoz et al. 2000). The great historical breakthroughs in the treatment of mood disorders can focus mainly on the discovery and therapeutic utilization of tricyclic antidepressants (ADTs) (Fangmann et al. 2008) and monoamine-oxidase inhibitors (MAOIs) (López-Muñoz et al. 2007) as antidepressants in the 1950s, and in the de˜nitive application of lithium salts in the treatment and prophylaxis of bipolar disorders during the 1960s (López-Muñoz et al. 2005). The introduction of the so-called atypical antidepressants, heterocyclic of the “second generation” (maprotiline, nomifensine, trazodone, and mianserine, among others) during the 1970s did not, contrary to what was thought at that time, assume transcendental advances from the therapeutic point of view nor from its safety pro˜le, except in individual cases, with respect to classic antidepressants. However, from the end of the 1980s, the addition to the antidepressant arsenal of a series of new families of drugs has contributed a therapeutic advance in some cases and, in others, a disappointment in the treatment of depression. As positive events among these new antidepressants we can consider, above all, selective serotonin reuptake inhibitors (SSRI), as well as noradrenaline and serotonin reuptake
22.1 Introduction .......................................................................................................................... 455 22.2 From Synaptic Pharmacology to Intraneuronal Pharmacology ........................................... 459 22.3 Postreceptor Mechanisms of Intracellular Transduction as Action Targets of
Antidepressant Drugs ........................................................................................................... 461 22.3.1 Role of GP ................................................................................................................. 462 22.3.2 Role of PKs ...............................................................................................................463 22.3.3 Role of CREB ...........................................................................................................464
