Considering the evident correlation between epileptogenesis and brain inflammation, and transient receptor potential vanilloid 1 (TRPV1) receptors involvement in inflammatory pain; we aimed at investigating possible involvement of the TRPV-1 receptors in acute pain in genetic model of absence epileptic WAG/Rij rats which has been shown to have increased nociceptive pain sensitivity (1). We also analyzed levels of IL-1β which is a pro-inflammatory cytokine which has been implicated to be involved in inflammatory conditions including inflammatory pain. Adult male WAG/Rij rats were utilized for the study. Tissue samples were collected from peripheral and central pain pathways involving dorsal root ganglion (DRG), trigeminal ganglia (TG), reticular thalamic nucleus (RTN) and anterior cingulate cortex (ACC). Expression and levels TRPV1 and IL-1 beta were assessed by real-time polymerase chain reaction (RT-PCR) method. The PCR products are expressed in relative to respective control values. Following stimulation with zymosan, expression of TRPV1 was determined to be significantly higher in TG (1.7 times, P<0.05), RTN (1.6 times, P<0.05) and ACC (3.4 times, P<0.05) but the increase in DRG was not statistically significant (n=8, for each). In addition, the expression of IL-1β was also significantly higher in TG, RTN, ACC and DRG (n=8). Data from this study provide evidence for a prominent acute inflammatory response and TRPV1 receptors plays a significant role in inflammatory hyperalgesia in absence epileptic rat model.