神经生长因子诱导的机械性痛觉过敏的线粒体依赖性。
Mitochondrial dependence of nerve growth factor-induced mechanical hyperalgesia.
机构信息
Department of Oral and Maxillofacial Surgery, University of California, San Francisco, CA, USA Division of Neuroscience, University of California, San Francisco, CA, USA Department of Medicine, University of California, San Francisco, CA, USA.
出版信息
Pain. 2011 Aug;152(8):1832-1837. doi: 10.1016/j.pain.2011.03.034. Epub 2011 May 12.
Abstract
Mitochondria are present at high concentration at the site of sensory transduction in the peripheral terminals of nociceptors. Because nerve growth factor (NGF), which induces nociceptor sensitization by acting on the high-affinity tropomyosin receptor kinase A (TrkA) receptor, also produces local recruitment of mitochondria in DRG neurons, we evaluated the role of mitochondria in NGF-induced mechanical hyperalgesia. Inhibition of 3 major mitochondrial functions-oxidation of nutrients, adenosine triphosphate (ATP) production, and generation of reactive oxygen species--markedly attenuated NGF-induced mechanical hyperalgesia in the rat. Disruption of microtubules, which are required for the trafficking and subcellular localization of mitochondria, also attenuated NGF-induced hyperalgesia. Our results suggest a contribution of mitochondrial localization and function to NGF-dependent pain syndromes.
摘要
线粒体在伤害感受器的外周末端的感觉转导部位高度集中。由于神经营养因子（NGF）通过作用于高亲和力原肌球蛋白受体激酶 A（TrkA）受体诱导伤害感受器敏化，也会导致 DRG 神经元中线粒体的局部募集，因此我们评估了线粒体在 NGF 诱导的机械性痛觉过敏中的作用。抑制 3 种主要的线粒体功能——营养物质的氧化、三磷酸腺苷（ATP）的产生和活性氧的产生——显著减弱了大鼠 NGF 诱导的机械性痛觉过敏。破坏微管，这是线粒体运输和亚细胞定位所必需的，也减弱了 NGF 诱导的痛觉过敏。我们的结果表明线粒体定位和功能对 NGF 依赖性疼痛综合征有一定的影响。
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