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Recording the MeA-VMHvl circuit involved in social defense: an optogenetic-assisted circuit mapping approach

Grant number: 24/01864-3
Support Opportunities:Scholarships abroad - Research Internship - Doctorate (Direct)
Effective date (Start): June 01, 2024
Effective date (End): May 31, 2025
Field of knowledge:Biological Sciences - Morphology - Anatomy
Principal Investigator:Simone Cristina Motta
Grantee:Alicia Moraes Tamais
Supervisor: Ruediger Klein
Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Research place: Max Planck Institute For Biological Intelligence, Germany  
Associated to the scholarship:22/07530-4 - Role of the medial amygdala nucleus in the re-exposure to social defeat, BP.DD

Abstract

During agonistic encounters among rodents, an important social cue for the expression of defense is the olfactory cues. Identifying the dominant conspecific and executing the defensive behavior appropriately is decisive for the survival of the individual. Regarding olfactory cues, pheromones are essential molecules for transmitting information about a conspecific, which are processed by the medial nucleus of the amygdala (MeA). The MeA projects to different regions that draw up the sexually dimorphic circuit of the hypothalamus, which regulates different types of social behaviors. An important target of MeA is the ventrolateral part of the ventromedial nucleus of the hypothalamus (VMHvl), which is responsible for organizing active defense in male mice. Previous work from our laboratory has shown that GABAergic and glutamatergic neurons from MeA differentially project to the VMHvl. GABAergic neurons, which are predominantly in posterodorsal MeA (MeApd), project to the VMHvl shell, which is composed of GABAergic neurons that tonically inhibit the glutamatergic core of the VMHvl. Glutamatergic neurons, which are mainly found in posteroventral MeA (MeApv), project to the VMHvl core, which is essentially composed of glutamatergic neurons and plays an important role in the expression of active defense. Based on these projection data and functional studies carried out in our laboratory, we hypothesize that activation of both GABAergic and glutamatergic neurons in MeA leads to activation of glutamatergic neurons in VMHvl, which leads to the expression of active defense. While the GABAergic neurons of the MeA would act through a disinhibition pathway involving the VMHvl shell, the glutamatergic neurons would directly stimulate the VMHvl core. To test our hypothesis of how MeA impacts VMHvl, we intend to use the channelrhodopsin-assisted circuit mapping technique, which combines optogenetics stimulation and whole-cell patch clamp. During the internship period with the group of Prof. Rüdiger Klein of the Max Planck Institute for Biological Intelligence, we plan to collaborate on ongoing projects and carry out the project proposed here.

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