Effects of exercise-induced increases in brain uptake of serum IGF-1 on raphe nuclei-hippocampal circuitry: implication on adult neurogenesis and mood homeostasis.

Abstract

Depression has emerged over the past decades as a leading cause of disability worldwide with a high prevalence in western populations, resulting in profound socioeconomic burden. Although the etiology of depression remains elusive, a growing body of evidence has indicated that disturbances in processes such as neurogenesis, monoaminergic neurotransmission and neurotrophic factor signaling may be involved in the physiopathology of this mood disorder. Several studies have reported the ability of physical exercise to counteract the depressive-like behaviors in depressed patients and in animal models. Importantly, it has been suggested that the antidepressant property of physical exercise require the participation of the serotonergic system and the IGF-1 pathway, both also implicated in exercise-induced hippocampal neurogenesis. Therefore, the aim of the present project is to verify whether increased uptake by the brain of circulating IGF-1 produced during exercise can modulate the activity of serotonergic raphe neurons and, consequently, increase serotonin signaling in the hippocampus to promote adult hippocampal neurogenesis and antidepressant effects.