Role of the medial amygdala nucleus in the re-exposure to social defeat

• Grant number: 22/07530-4
• Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
• Effective date (Start): December 01, 2022
• Status: Discontinued
• Field of knowledge: Biological Sciences - Morphology - Anatomy
• Principal Investigator: Simone Cristina Motta
• Grantee: Alicia Moraes Tamais
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated research grant: 16/18667-0 - Manipulating the neural circuit underlying social defense, AP.JP
• Associated scholarship(s): 24/01864-3 - Recording the MeA-VMHvl circuit involved in social defense: an optogenetic-assisted circuit mapping approach, BE.EP.DD

Abstract

During agonistic encounters between rodents, an important social cue for defense expression is olfactory. Identifying the dominant conspecific and performing the defensive behavior properly is decisive for the individual's survival. In nature, individuals face conspecific dominants throughout their lives. Thus, although it is an innate type of behavior, the social defense can be shaped and expressed through defensive strategies that are more advantageous to the individual according to experience. Previous work from our laboratory verified a change in the defensive behavior pattern and the activation of brain areas in mice exposed to repeated encounters with an aggressive conspecific. Repeatedly defeated animals have longer passive defense time and less activation of the medial amygdala nucleus (MeA). As it is a brain structure that acts by processing olfactory sensory information from the vomeronasal organ (VNO) and accessory olfactory bulb (AOB), and which densely projects to regions of the hypothalamus involved with the execution of defensive behavior, the lower MeA activation may be involved with the behavioral adaptation process observed in animals repeatedly defeated by the aggressor animal. Furthermore, as MeA has a wide expression of receptors for neuromodulators and hormones, the reduction in MeA activity may be due to plasticity in MeA neurons by the action of a modulator. In this sense, several works place oxytocin as an important neuromodulator acting on the salience given to olfactory information in MeA. Thus, the objective of this project is to investigate the role of MeA and the influence of oxytocin in the remodeling of defensive behavior during repeated agonistic encounters. For this, we will use tools for mapping the neural populations of MeA involved in the defensive response, functional manipulation of specific neural populations, methods for in vivo monitoring of the activity of these populations, and techniques for controlling the release of oxytocin. (AU)