Role of fluoxetine on depression-related pathophysiological mechanisms

Abstract

Major depression is a very common and serious mood disorder characterized by heterogeneous etiopathology. Treatment of the disease usually involves the use of antidepressant medications whose basic mechanism is achieved via increasing synaptic levels of monoamine neurotransmitters in different brain regions affected by the disease. Currently used antidepressant medications display limited efficacy with a pronounced delay to onset of action, and they all provoke disturbing side effects. With the ultimate goal of uncovering the primary postsynaptic actions that may initiate cellular antidepressive signaling, basic and clinical researches are devoted to studying the effects of antidepressants, particularly those most commonly used, selective serotonin reuptake inhibitors (SSRIs), on the complex signaling network that is known to be altered in depression. This includes the effects of antidepressants on the hypothalamic-pituitaryadrenal axis (HPA) activity, production of neurotrophins and regulation of neurogenesis, pro-inflammatory and anti-inflammatory cytokines, oxidative stress and mitochondrial functioning. Herein, we discuss the latest published data from animal and clinical studies that have examined the effects of different SSRIs on depression-related pathophysiological mechanisms. Special attention will be dedicated to gender-specific effects of SSRIs action and to their adverse effects. © 2015 by Nova Science Publishers, Inc. All rights reserved.