Neuronal mechanisms of social behaviours

Speaker: Felix Leroy, Ph.D. 

Instituto de Neurociencias en Alicante 

Biography of the speaker:  

Felix Leroy is a neuroscientist studying the neural basis of social interactions. Following his bachelor and master degrees at the Ecole Normale Supérieure, he received a Ph.D. in neuroscience with Suma Cum Laude from the Paris Descartes University in 2014. For his post-doctoral studies, he joined the laboratory of Steven Siegelbaum at Columbia University. He became interested in a little-studied hippocampal region named CA2 that is necessary for social memory. After discovering a new form of plasticity in CA2 that may support social memory encoding (Leroy et al., Neuron 2017 ; Leroy et al., Molecular Psychiatry 2021), he began examining how CA2 output could regulate social behaviors. Based on his finding that CA2 sends a strong projection to the lateral septum, an area implicated in aggression, he focused on how CA2 might modulate social aggression. As a core motivated behavior, aggression is controlled by a hypothalamic nucleus, specifically the ventro-lateral part of the ventro-medial hypothalamic nucleus (VMHvl). He discovered that CA2 upregulates VMHvl activity, thereby enhancing aggression, through a disynaptic disinhibitory circuit in the lateral septum that is modulated by the social neuropeptide arginine vasopressin (Leroy et al. Nature 2018). In addition, he contributed to several other studies exploring the role of the CA2 to ventral CA1 projection in social memory (Meira, Leroy et al. Nature Communication 2018) or how sharp-wave ripples originating from CA2 could regulate the formation of social memory (Oliva, Ruiz, Leroy et al., Nature 2020). In the Fall of 2020, he joined the Instituto de Neurociencias de Alicante (the largest Spanish neuroscience institute managed by the Consejo Superior de Investigaciones Cientificas and the Universidad Miguel Hernández ) as Principal Investigator. He is leading the cognition and social interactions laboratory where they investigate how social cognition (past experiences and decisions) prioritize, determine and calibrate innate social behaviors. Indeed, while the cognitive functions of the cortex (neocortex and hippocampus) have been extensively studied, we know much less about its ability to regulate motivated behaviors fulfilling physiological, safety and social needs. The lateral septum (LS) is ideally positioned to integrate cortical signals in order to regulate the activity of hypothalamic and midbrain nuclei controlling motivated behaviors. LS also receives numerous modulatory inputs from subcortical brain regions. Based on recent cortical-LS-subcortical circuit studies, they study how LS integration of cognitive inputs regulates motivated behaviors. This is all the more important since malfunctions occurring within cortical-LS circuits may lead to altered social behaviors, a hallmark of many psychiatric disorders. In a recent publication from his laboratory, they elucidated a novel circuit whereby release of CRH in the septum from the prefrontal cortex suppresses social interactions with familiar mice and therefore promote social novelty preference (de Leon Reyes et al., Cell 2023). In addition, maturation of the circuit also allows a shift in social preference in young mice from familiar to novel animals. 

Description of the general focus of the symposium:  

Social behavior, defined broadly as any form of physical interaction or non-physical communication between members of the same species, represents one of the most powerful drivers of behavior across mammals. It encompasses diverse interactions, including mating, parental care, aggression, and affiliation. Aggressive behaviors establish dominance hierarchies and regulate access to resources, while affiliative behaviors, such as grooming and cooperation, promote cohesion and reduce conflict. Social structures emerge from ecological pressures such as resource distribution, predation risk, and habitat organization, which shape the costs and benefits of group living. Much like physiological drives such as hunger or sleep, social needs are homeostatically regulated. In humans, altered social responsiveness and disrupted social motivation characterize several neuropsychiatric disorders, including autism spectrum disorder, schizophrenia, and psychopathy, all of which involve dysfunction in social reward processing. In rodents, unmet social needs have profound consequences: social deprivation causes long-term social, cognitive, emotional and metabolic impairments. Thus, maintaining social connectedness is not merely advantageous but biologically essential, supporting adaptive behavior and mental health. Despite their importance, the neurobiological mechanisms underlying the formation and maintenance of peer relationships remain largely unexplored. The symposium presents the latest research on the mechanisms controlling social behavior, focusing on pathways that control motivation driving social interactions and the rewarding effects of social contact. 

Brief description of the talk:  

Neuronal circuits regulating social preferences: social preference, the decision to interact with one conspecific over another, is a feature displayed by gregarious animals which is critical to navigate their social space. Thus, adult rodents prefer to interact with their kin, individuals from specific strains and members of the opposite sex. In addition to innate factors (e.g., kin, strain, and sex), social preference is also influenced by social memory, social hierarchy and the affective state of the conspecific. In the lecture, I will explore brain pathways and neuronal mechanisms controlling social preference.