Social anxiety disorder (SAD) involves excessive fear of social situations and can be induced by social trauma. However, the underlying mechanisms of individual differences in the formation of social fear memory remain unclear. To address this gap, we adapted our mouse social fear conditioning paradigm for rats (rSFC) and compared adult male rats selectively bred for high (HAB) or low (LAB) anxiety-related behaviour and non-selected controls (NAB). HAB and LAB rats are established as a model displaying genetically determined extremes in socio-emotional behaviours. Conditioned HAB, LAB, and NAB rats all developed social fear, but with line-specific persistence. During a social fear discrimination test, HAB and LAB rats expressed social fear 24 h after acquisition, while NAB rats only showed transient social fear (up to 6 h), indicating reduced susceptibility to social trauma. Importantly, only HAB rats showed individual social fear memory, with reduced social investigation of the familiar rat encountered during social fear acquisition (“known”) versus a novel (“unknown”) rat. Blockade of brain V1a receptors after social fear acquisition slightly reduced generalised social fear in HAB rats and abolished their individual social fear memory, whereas central infusion of arginine vasopressin (AVP) modestly reduced generalised social fear in LAB rats. Additionally, rSFC induced a rapid corticosterone response, which was more pronounced in NAB than HAB rats. Blocking glucocorticoid synthesis before social fear acquisition slightly reduced generalised social fear in HAB rats. These findings demonstrate that innate anxiety determines the long-term formation of individual social fear memory, as assessed after a 24-h retention interval, in adult male rats and support rSFC as a useful experimental model to investigate selected neurobiological mechanisms relevant to SAD.