Importance of post-training paradoxical sleep for context-conditioned fear response

• Grant number: 08/10148-7
• Support Opportunities: Scholarships in Brazil - Doctorate
• Effective date (Start): April 01, 2009
• Effective date (End): March 31, 2013
• Field of knowledge: Biological Sciences - Pharmacology - Neuropsychopharmacology
• Principal Investigator: Deborah Suchecki
• Grantee: Carlos Eduardo Neves Girardi
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Posttraumatic Stress Disorder (PTSD) is an anxiety disorder that results from exposure to a traumatic event, such as, violent crimes, war and natural disasters. There is growing evidence that sleep disruption that occurs following trauma exposure may constitute a specific mechanism involved in the pathophysiology of chronic PTSD. Processes that occur during the sleep that follows trauma may represent a natural protection against PTSD. It is suggested that distinctive symptoms of PTSD are a result of an inadequate processing of the emotional memory related to the traumatic event, whilst long post-trauma REM sleep periods would favor the processing of these memories, preventing the progression of the disorder. In this project, we will use a paradigm of early life adverse event that interferes with the ontogenesis of the stress response, as a potential model for studying the possible commitment in the sleep rebound mechanism following intense paw-shock stress in order to assess the importance of sleep for traumatic emotional memory consolidation (considering paw shock at the intensity used, 2mA for 10s, as being traumatic). For this purpose, early-life mother deprived rats will be submitted to a trauma (paw-shock fear conditioning) in adulthood and the subsequent sleep will be recorded to evaluate whether the amount of paradoxical sleep (PS) following the trauma correlates with freezing behavior upon conditioning-context re-exposure. Furthermore, we will perform pharmacological manipulations in order to induce or impair PS following trauma and to interfere on the potential influence of PS on conditioned fear. Therefore, we aim to contribute to the elucidation of the functions of post-trauma PS in the processing of emotional memory, and thus, extrapolate these results to PTSD in order to propose new prevention strategies for this disorder.