THE DORSAL AND VENTRAL HIPPOCAMPUS CAUSALLY REGULATE DISTINCT ASPECTS OF RESCUE BEHAVIOR AND NETWORK COACTIVITY IN MICE

Prosocial behavior, such as rescuing conspecifics in distress, is fundamental component of social interaction across species. We investigated the neural basis of this behavior in mice using a rescue behavior task (RBT). Observer mice learned to release a victim trapped in a box containing cold water (CW) or a dry box (Social Separation, SS). We found that high-stress contexts (CW) significantly accelerated the rescue compared to SS, independent of sex. To dissect the hippocampal contribution, we employed chemogenetic silencing. Inhibition of the dorsal hippocampus (dHPC) throughout training prevented rescue acquisition. In contrast, silencing the ventral hippocampus (vHPC) did not impair rescue performance but significantly altered post-liberation social engagement.This suggests a functional dissociation, with the dHPC supporting task learning and the vHPC modulating social processing. We further examined downstream network effects via brain-wide c-Fos mapping. Inter-regional functional correlations and graph-theory analysis showed that dHPC silencing disrupted coactivity patterns between cognitive and emotional regions, shifting the network topology from a dHPC-mediated state to a basolateral amygdala-centric state. These results suggest that the dHPC is essential for integrating spatial and social information during rescue learning, whereas vHPC inhibition influences brain-wide neural activity through distinct mechanisms. Building on this dissociation, our ongoing research utilizes a post-traumatic stress disorder (PTSD) model to determine if prosocial actions can ameliorate stress responsivity and facilitate resilience in traumatized individuals. Using Calcium imaging and engram labeling, we examine the vHPC by tracking neuronal ensembles engaged during both trauma and helping, to determine the neural networks linking these processes.