In modern society, stress is considered a crucial determinant to influence various aspects of individuals’ life, including sociability, in which the role of oxytocin has been recognized to benefit social bonding or provides a buffering effect. However, the relationship between stress-induced fear and oxytocin-associated social behavior is not clear, particularly when individual encounters situation with similar context of the stressful event. The present study targeted at this issue by examining whether acute restraint stress (ARS) may change the profiles of anxiety (indexed by elevated T maze, ETM) and prosocial behavior (indexed by social choice test, SCT), and were these ARS effects can be adjusted by the pharmacological intervention of L-368899, an oxytocin antagonist and antalarmin, a corticotropin-releasing hormone (CRH) receptor antagonist. Peripheral corticosterone and the tissue levels of serotonin (5-HT), dopamine (DA), and norepinephrine (NE) in hippocampus, medial prefrontal cortex (mPFC), and amygdala were measured to manifest rats’ anxiety tone and the disturbance of monoaminergic neural substrates in fear circuit. Our results showed that: (i) ARS rats more frequently chose the chamber with prosocial opportunity, and L-368899 and antalarmin were found to undo this effect. (ii) ARS rats were found to have a lower DA but higher NE levels in mPFC, both can be reversed by L-368899. (iii) ARS rats were found to have a lower level of corticosterone, together with shorter avoidance latency and longer escape latency of ETM. Our results may contribute to the understanding of stress-related sociability and the context-dependent role of oxytocin.