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炎症性疼痛大鼠模型中一氧化氮合酶相互作用蛋白NOSIP的脊髓上调

Spinal upregulation of the nitric oxide synthase-interacting protein NOSIP in a rat model of inflammatory pain.

作者信息

Dreyer Jacqueline, Hirlinger David, Müller-Esterl Werner, Oess Stefanie, Kuner Rohini

机构信息

Department of Molecular Pharmacology, Pharmacology Institute, University of Heidelberg, Im Neuenheimer Feld 366, 69120 Heidelberg, Germany.

出版信息

Neurosci Lett. 2003 Oct 16;350(1):13-6. doi: 10.1016/s0304-3940(03)00771-7.

Abstract

Nitric oxide and nitric oxide synthases are key players in synaptic plasticity events in the spinal cord, which underly the development of chronic pain states. To date, little is known about the molecular mechanisms regulating the activity of nitric oxide synthases in nociceptive systems. The present study was aimed at the immunohistochemical determination of the expression of a nitric oxide synthase-interacting protein (NOSIP) in the rat spinal cord and dorsal root ganglia and studying its regulation in states of nociceptive hypersensitivity in a rat model of post-inflammatory pain. NOSIP is predominantly expressed in nociceptive primary neurons and in neurons of the spinal dorsal horn and the number of NOSIP-positive spinal neurons increases significantly following induction of unilateral intraplantar injection of complete Freund's adjuvant. Thus, NOSIP may modulate nitric oxide homeostasis in physiological and pathological pain conditions.

摘要

一氧化氮和一氧化氮合酶是脊髓突触可塑性事件中的关键参与者,这些事件是慢性疼痛状态发展的基础。迄今为止,关于调节伤害性感受系统中一氧化氮合酶活性的分子机制知之甚少。本研究旨在通过免疫组织化学方法测定大鼠脊髓和背根神经节中一氧化氮合酶相互作用蛋白(NOSIP)的表达,并研究其在炎症后疼痛大鼠模型中伤害性超敏状态下的调节情况。NOSIP主要表达于伤害性初级神经元以及脊髓背角神经元,在单侧足底注射完全弗氏佐剂诱导后,NOSIP阳性脊髓神经元数量显著增加。因此,NOSIP可能在生理和病理疼痛状态下调节一氧化氮的稳态。

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