Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Sensitization of dural afferents underlies migraine-related behavior following meningeal application of interleukin-6 (IL-6) | Yan et al. Molecular Pain 2012 8 6 http content 8 1 6 MOLECULAR PAIN RESEARCH Open Access Sensitization of dural afferents underlies migraine-related behavior following meningeal application of interleukin-6 IL-6 Jin Yan1 Ohannes K Melemedjian1 Theodore J Price1 2 3 and Gregory Dussor1 2 Abstract Background Migraine headache is one of the most common neurological disorders but the pathophysiology contributing to migraine is poorly understood. Intracranial interleukin-6 IL-6 levels have been shown to be elevated during migraine attacks suggesting that this cytokine may facilitate pain signaling from the meninges and contribute to the development of headache. Methods Cutaneous allodynia was measured in rats following stimulation of the dura with IL-6 alone or in combination with the MEK inhibitor U0126. The number of action potentials and latency to the first action potential peak in response to a ramp current stimulus as well as current threshold were measured in retrogradely-labeled dural afferents using patch-clamp electrophysiology. These recordings were performed in the presence of IL-6 alone or in combination with U0126. Association between ERK1 and following IL-6 treatment was also measured by co-immunoprecipitation. Results Here we report that in awake animals direct application of IL-6 to the dura produced dose-dependent facial and hindpaw allodynia. The MEK inhibitor U0126 blocked IL-6-induced allodynia indicating that IL-6 produced this behavioral effect through the MAP kinase pathway. In trigeminal neurons retrogradely labeled from the dura IL-6 application decreased the current threshold for action potential firing. In response to a ramp current stimulus cells treated with IL-6 showed an increase in the numbers of action potentials and a decrease in latency to the first spike an effect consistent with phosphorylation of the sodium channel . Pretreatment with U0126 reversed hyperexcitability following IL-6 treatment. .
