Role of corticolimbic glucocorticoid receptor signaling in traumatic stress pathology

• Grant number: 23/00282-8
• Support Opportunities: Scholarships abroad - Research Internship - Post-doctor
• Start date: May 01, 2023
• End date: April 30, 2024
• Field of knowledge: Biological Sciences - Pharmacology - Neuropsychopharmacology
• Principal Investigator: Cleopatra da Silva Planeta
• Grantee: Leandro Augusto de Oliveira
• Supervisor: James Paul Herman
• Host Institution: Faculdade de Ciências Farmacêuticas (FCFAR). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil
• Institution abroad: University of Cincinnati, United States
• Associated to the scholarship: 19/25035-8 - Study of the involviment of CRF binding protein (CRFBP) into medial prefrontal cortex (mPFC) on control of cardiovascular, neuroendocrine and behavioral responses evoked by acute and chronical psychological stress in rats, BP.PD

Abstract

Post-traumatic stress disorder (PTSD) is shown to increase the sensitivity of glucocorticoid signaling through glucocorticoid receptor. Furthermore, is related to disfunction of brain structures associated to fear response. Homologous circuits such as infralimbic cortex (IL) to basolateral amygdala (BLA), produces extinction and reinstatement deficits in rodents. While the PTSD-related GR dysfunction is shown in rats, the brain mechanisms are poorly understood. This project will test the hypothesis that hormonal responsiveness to stress and trauma are critical for susceptibility to generate behavioral pathologies, including the PTSD. Will use pharmacological, genetic, electrophysiological and machine learning approaches to provide novel insight into our understanding of the role of glucocorticoid signaling in genesis of pathological fear and anxiety. Specifically, will investigate the role of GR signaling in IL pyramidal cell populations in state variable in acquisition and extinction of conditioned fear, development of aberrant threat assessment/avoidance strategies and cognitive dysfunction following exposure to single Prolonged Stress (SPS). Furthermore, will investigate the GR signaling within the IL to BLA connection in driving SPS-related state variable in acquisition and extinction of conditioned fear, development of aberrant threat assessment/avoidance strategies and cognitive dysfunction. (AU)