לוח שנה משולב

What are the neural processes that lead to a decision to approach another individual in need and help them out of a tight spot? Multiple factors weigh in on this decision, including empathic arousal and social identity. The drive to act prosocially in response to others distress is evolutionarily rooted in mechanisms underlying parental behavior and group living. In humans, helping involves socio-emotional and cognitive components, and recruits brain regions involved in affective empathy arousal, executive function and motivation. This talk will present an overview of the rat Helping Behavior Test, which investigates the complex response leading to rescue of trapped conspecifics, and examine evidence to ask whether similar capacities are involved in rat helping. We’ll explore the idea that rat helping is motivated by empathy, what is the difference between social and prosocial reward, and whether helping is motivated by valuation of others’ outcomes. I will share what we’ve learned about the distinct neural network that is associated with empathy and prosocial behavior, and discuss findings of ingroup bias, adolescent helping, and interactions with rat immune function and wellbeing. We’ll ask what is the link between prosocial motivation and aggression, and what is the role of the social group in these behaviors.

Osteoclasts are bone degrading cells, notorious for their role in osteoporosis (a bone disease characterized by decreased density and structural deterioration). However, complete absence of osteoclast activity can be lethal, and optimal bone health relies on remodeling, where osteoclasts resorb old bone and osteoblasts rebuild it. Osteoclasts are large multinucleated cells that form through cell-cell fusion of their precursors. This fusion process is crucial for osteoclast differentiation, but it is not completely understood. New insights into this process could enable development of advanced pharmaceuticals that can fine-tune osteoclast activity. Using mutants derived from a lethal genetic bone disease, we discovered a unique phenotype: osteoclasts that never stop fusing, creating huge cells that are also paradoxically inactive in resorbing bone. I will discuss the genes involved, and our recent results and hypotheses about this intriguing molecular mechanism.