|Support type:||Scholarships in Brazil - Scientific Initiation|
|Effective date (Start):||March 01, 2020|
|Effective date (End):||December 31, 2020|
|Field of knowledge:||Biological Sciences - Pharmacology - Neuropsychopharmacology|
|Principal Investigator:||Carlos Cesar Crestani|
|Grantee:||Camila Marchi Coelho|
|Home Institution:||Faculdade de Ciências Farmacêuticas (FCFAR). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil|
Studies in humans and animals have provided evidence correlating stress with the pathogenesis of several psychiatric disorders, including depression. Despite the relevance of these findings, neurobiological mechanisms related to stress-evoked behavioral changes are still poorly understood. The amygdaloid complex is an important limbic structure involved in the physiological and behavioral responses to stress. A sub-nucleus of the amygdaloid complex activated during stress is the medial nucleus (MeA). The involvement of MeA in the modulation of depressive-like behaviors in rodents has been demonstrated, but the possible involvement of this amygdaloid nucleus in the behavioral responses evoked by exposure to aversive threats has never been investigated. In addition, local neurochemical mechanisms involved in controlling behavioral responses to stress are also poorly understood. In this sense, angiotensin II acting through the AT1 receptor has been shown to be an important neurochemical mechanism in the central nervous system involved in the etiology of behavioral changes and physiological adjustments during exposure to aversive situations; whereas the action of angiotensin II on the AT2 receptor appears to be a counterregulatory mechanism for the pro-stress effects of the AT1 receptor. Data also showed that stress exposure alters the formation of angiotensin II and the expression of the AT1 receptor in the central nervous system. The neurotransmission angiotensin 1-7/receptor Mas is also reported as a counterregulatory mechanism of the renin-angiotensin system for the pro-stress effects of angiotensin II/AT1 receptor neurotransmission. In fact, intracerebroventricular administration of angiotensin 1-7 has been shown to decrease stress-evoked physiological and behavioral responses. Despite these pieces of evidence, the specific sites in the brain where angiotensin II and angiotensin 1-7 act to control stress responses are not fully understood. Angiotensinergic terminals and components of RAS (e.g, angiotensinogen, and angiotensin II and angiotensin 1-7 receptors) were identified within the MeA. However, a possible involvement of MeA angiotensinergic neurotransmissions in stress-evoked behavioral responses has never been investigated. Thus, our proposal in the present study is: 1) to assess the involvement of the AT, AT and Mas receptors into the MeA in behavioral changes in the forced swimming test induced by exposure to an acute session of restraint stress in rats; 2) to investigate the role of AT, AT and Mas receptors into the MeA in behavioral changes in the forced swimming test induced by exposure to a protocol of repeated restraint stress.