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The importance of glucocorticoid receptors in late anxiety and dendritic remodeling in BLA induced by acute stress in rats

Grant number: 16/21559-4
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): January 01, 2017
Effective date (End): December 31, 2017
Field of knowledge:Biological Sciences - Pharmacology
Principal Investigator:Carolina Demarchi Munhoz
Grantee:Letícia Morais Bueno de Camargo
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Anxiety-related disorders are common among the psychiatric patients and are widely present in studies devoted to stress, which use different approaches to investigate the neurobiological mechanisms underlying the persistence of anxiety symptoms caused by a stressful event. It is well known that acute restraint stress or increased serum levels of glucocorticoid (GC) stress hormones induce not only long-lasting anxiety (measured 10 days after stressor stimulus or GC infusion) but also remodeling of dendritic branches in basolateral amygdala complex (BLA) in rats. Recently, we found that exposure to environmental enrichment (EE) prevented anxiety-related behavior in adult rats precipitated immediately after acute restraint stress. This protective role of EE on stress-induced anxiety seems to be due to the prevention of the stress-induced increase in glucocorticoid receptor (GR) nuclear activity in the basolateral nucleus of the amygdala (BLA). In a more recent work, we showed that EE is also able to prevent the restraint stress-induced long-lasting anxiety (10 days after stress) in rats, but it is not yet clear if this protective effect of EE is dependent of changes in GR nuclear activity in the BLA. Moreover, recent data from our group showed that prior injection (systemically) of metyrapone (a GC synthesis inhibitor) prevented the long-last anxiety behavior triggered by acute immobilization (2h), suggesting a key role of this hormone in the anxiogenic effect of stress. To determine whether the effects of stress in anxiety-like behavior and in the dendritic branch remodeling in the BLA are dependent GR signaling, we propose in this project antagonize the genomic (over-expressing a dominant negative form of GR - tdGR, via viral vector) and non-genomic (by administration of the GR antagonist RU486) action of this receptor in the BLA during the acute stress immobilization. (AU)