Deep Brain Stimulation in Major Depression: Plastic Changes of 5-Hydroxytryptamine Neurons

Abstract

Major depressive disorder (MDD) is a severe psychiatric syndrome with a very high socioeconomic impact. The high cost of MDD is attributable to its large incidence in the general population (lifetime prevalence is close to 20%); the long duration of depressive episodes; and emergence of depressive episodes during active periods of adult life, which results in very large labor costs. The large and increasing impact of MDD is not paralleled by marked improvements in its treatment. The antidepressant market is dominated by drugs targeting the monoamine systems, such as selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors, which are pharmacologic refinements of tricyclic antidepressant drugs, which were discovered serendipitously in the 1950s. Selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors have increased treatment compliance because of the absence of severe side effects. However, their speed and efficacy are suboptimal, leaving a large percentage of patients with partial or incomplete responses after several months of treatment. Many patients are refractory to numerous pharmacologic treatments and require nonstandard interventions to improve their quality of life and reduce suicide risk. Antidepressant-like Effects of Cortical Deep Brain Stimulation Coincide With Pro-neuroplastic Adaptations of Serotonin SystemsBiological PsychiatryVol. 76Issue 3PreviewCortical deep brain stimulation (DBS) is a promising therapeutic option for treatment-refractory depression, but its mode of action remains enigmatic. Serotonin (5-HT) systems are engaged indirectly by ventromedial prefrontal cortex (vmPFC) DBS. Resulting neuroplastic changes in 5-HT systems could thus coincide with the long-term therapeutic activity of vmPFC DBS. Full-Text PDF ErratumBiological PsychiatryVol. 76Issue 5PreviewErratum to: “Deep Brain Stimulation in Major Depression: Plastic Changes of 5-Hydroxytryptamine Neurons” by Artigas which appeared in Biological Psychiatry (2014;76:174-175). On page 175, column 1, 8th line from the bottom, the findings were inadvertently misstated as a decrease rather than an increase. The full corrected sentence is: “Using this procedure, the authors found that CSDS induced a robust and significant increase of the density of 5-HT nerve endings in various forebrain areas, including the vmPFC, the basolateral amygdala, and the dentate gyrus of the hippocampal formation, which was normalized after long-term DBS treatment.” Full-Text PDF