Cognitive interventions, including distraction, have been successfully utilized in the manipulation of experimental pain and the treatment of clinical pain. Attentional diversions can reduce the experience of pain, a phenomenon known as distraction analgesia (DA). Prior research has suggested that variations in stimulus intensity may influence the magnitude of DA. However, the neural substrates of DA remain largely unknown. Converging evidence suggests that the infralimbic cortex (IL) in the brains of rats may contribute to the phenomenon of DA. The function of the rat IL in DA has never been directly investigated, therefore, this study sought to identify the role of the IL at two levels of noxious stimulus intensity among brain-intact and IL lesioned male rats within an established rat model of DA. A distractor object reduced formalin-induced nociceptive behavior in brain-intact rats, and this DA effect was detectable during low- (.5% formalin) and high-intensity (1% formalin) stimulation. IL lesion resulted in a near-complete elimination of the DA effect and an overall reduction in formalin pain. These results provide the first known evidence that (i) the IL is involved in processing DA in rats, (ii) the IL contributes to formalin-induced nociceptive behavior irrespective of distraction, and (iii) a high-intensity stimulation was generally more susceptible to DA than low-intensity stimulation. These findings may further inform the mechanisms and future development of non-pharmacological strategies to reduce pain.