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The role of medial prefrontal cortex mineralocorticoid and glucocorticoid receptors in the process of extinction of aversive memory in rats submitted to acute stress

Grant number: 17/14473-9
Support type:Regular Research Grants
Duration: February 01, 2019 - January 31, 2021
Field of knowledge:Biological Sciences - Pharmacology
Principal Investigator:Leonardo Resstel Barbosa Moraes
Grantee:Leonardo Resstel Barbosa Moraes
Home Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil


The aim of the present study is to investigate the role of acute stress and mineralocorticoid and glucocorticoid receptors present in the prefrontal cortex in the memory extinction learning. For this purpose, male Wistar rats will submitted to a surgery for the implant of a radiotelemetric probe into the abdominal aorta for monitoring autonomic responses, and after, cannulae guide will be stereotaxically implanted bilaterally in in the infralimbic (IL) or prelimbic (PL) regions of the ventromedial prefrontal cortex (vmPFC) of rodents for drug administration. After recover from surgeries, the animals will be exposure to a single and brief session of an uncontrollable stress (restraint stress for 1 hour). On the seventh day after de acute restraint stress session they will be trained in contextual fear conditioning protocol, followed by extinction session and extinction retention session, all sessions with a 24 hour interval. The mineralocorticoid receptor antagonist (RU 23318), or glucocorticoid receptor antagonist (RU 486) or the vehicle will be administered to the animals by microinjections into the IL or PL, 10 minutes before or immediately after the extinction session. Our hypothesis is that the mineralocorticoid and glucocorticoid receptors are important for the extinction of aversive memory, and that acute stress produces a deficit in the conditioned fear extinction learning through changes in the expression of receptors for glucocorticoids in vmPFC, and morphological modifications in this brain structure. (AU)