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학술저널
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대한구강생물학회 International Journal of Oral Biology International Journal of Oral Biology 제34권 제1호
발행연도
2009.1
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1 - 6 (6page)

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The purpose of the present study was to examine the role of peripheral nitric oxide (NO) pathways in the onset of interleukin (IL)-1β-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-1β or other chemicals. We subcutaneously injected 50 μL of IL-1β into a vibrissa pad through the implanted polyethylene tube with a 100 μL Hamilton syringe. After the administration of 0.01, 0.1, 1, or 10 pg of IL-1β, 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-1β, the threshold of air puffs decreased significantly to 12 ± 3, 7 ± 2, 5 ± 1, or 5 ± 1 psi, respectively, in a dose dependent manner. Pretreatment with L-NAME, a nitric oxide synthase (NOS) inhibitor, blocked IL-1β-induced mechanical allodynia. However, neither D-NAME, an inactive isomer of LNAME, nor vehicle affected the IL-1β-induced mechanical allodynia. Subcutaneous injection of IL-1β 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 proinflammatory cytokines and NO are important contributors to the pathogenesis of persistent and exaggerated IL-1β-induced pain states. Based on these observations, peripheral application of NOS inhibitors may be of therapeutic value in treating pain disorders in the clinic.

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