The purpose of the present study was to examine the role of peripheral nitric oxide (NO) pathways in the onset of interleukin (IL)-1$eta$-induced mechanical allodynia in the orofacial area. Experiments were carried out on male Sprague-Dawley rats weighing 230-280 gm and surgical procedures were performed under pentobarbital sodium (40 mg/kg, i.p.). Under anesthesia, a polyethylene tube (PE10) was implanted into the subcutaneous area of one vibrissa pad, which enabled the injection of IL-1$eta$ or other chemicals. We subcutaneously injected 50 ${mu}L$ of IL-1$eta$ into a vibrissa pad through the implanted polyethylene tube with a 100 ${mu}L$ Hamilton syringe. After the administration of 0.01, 0.1, 1, or 10 pg of IL-1$eta$, withdrawal behavioral responses were examined. The subcutaneous injection of saline had no effects on the air-puff thresholds. Following the subcutaneous injection of 0.01, 0.1, 1, or 10 pg of IL-1$eta$, the threshold of air puffs decreased significantly to 12 $pm$ 3, 7 $pm$ 2, 5 $pm$ 1, or 5 $pm$ 1 psi, respectively, in a dose dependent manner. Pretreatment with L-NAME, a nitric oxide synthase (NOS) inhibitor, blocked IL-1$eta$-induced mechanical allodynia. However, neither D-NAME, an inactive isomer of L-NAME, nor vehicle affected the IL-1$eta$-induced mechanical allodynia. Subcutaneous injection of IL-1$eta$ increased the number of c-fos-like immunoreactive neurons, whereas pretreatment with L-NAME decreased this number, in the trigeminal caudal nucleus. These results suggest that pro-inflammatory cytokines and NO are important contributors to the pathogenesis of persistent and exaggerated IL-1$eta$-induced pain states. Based on these observations, peripheral application of NOS inhibitors may be of therapeutic value in treating pain disorders in the clinic.