Inflammatory mediators enhance the excitability of chronically compressed dorsal root ganglion neurons
Inflammatory mediators enhance the excitability of chronically compressed dorsal root ganglion neurons
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DOI：
10.1152/jn.00748.2005
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发表时间：
2006-04-01
影响因子：
2.5
通讯作者：
LaMotte, RH
中科院分区：
文献类型：
--
作者：
Ma, C;Greenquist, KW;LaMotte, RH
侧方椎间盘突出、椎管狭窄和各种脊柱退行性或创伤性疾病有时会导致背根神经节的慢性受压和炎症以及包括疼痛在内的慢性异常感觉。大鼠背根神经节（CCD）长期受压后，背根神经节（DRG）体细胞变得过度兴奋，有些表现出异位自发活动（SA）。炎症介质在调节 DRG 神经元的兴奋性方面具有潜在作用，因此可能导致 CCD 后神经元过度兴奋。在这项研究中，将由缓激肽、血清素、前列腺素E 2 和组胺（各10(-6) M）组成的炎症汤（IS）局部应用于DRG。 DRG 神经元的反应是在细胞外从被梳理的背根纤维或在细胞内从完整 DRG 中的体细胞或从培养 30 小时内分离的神经元进行电生理记录。在所有三种制剂中，IS 显着增加了 SA CCD 神经元的放电率，并在比对照神经元更多的沉默 CCD 中诱发放电。 IS 轻微地使静息膜电位去极化，并降低完整和解离神经元中动作电位的电流和电压阈值，尽管去极化或动作电位阈值降低的幅度在 CCD 和对照之间没有显着差异。在每个大小类别的一定比例的神经元中都发现了 IS 诱发的反应，包括具有和不具有伤害性特性的神经元。炎症介质通过增加 DRG 体的兴奋性，可能导致 CCD 诱导的神经元过度兴奋以及痛觉过敏和触觉异常性疼痛。
A laterally herniated disk, spinal stenosis, and various degenerative or traumatic diseases of the spine can sometimes lead to a chronic compression and inflammation of the dorsal root ganglion and chronic abnormal sensations including pain. After a chronic compression of the dorsal root ganglion (CCD) in rats, the somata in the dorsal root ganglion (DRG) become hyperexcitable, and some exhibit ectopic, spontaneous activity ( SA). Inflammatory mediators have a potential role in modulating the excitability of DRG neurons and therefore may contribute to the neuronal hyperexcitability after CCD. In this study, an inflammatory soup ( IS) consisting of bradykinin, serotonin, prostaglandin E 2, and histamine ( each 10(-6) M) was applied topically to the DRG. The responses of DRG neurons were electrophysiologically recorded extracellularly from teased dorsal root fibers or intracellularly from the somata in the intact DRG or from dissociated neurons within 30 h of culture. In all three preparations, IS remarkably increased the discharge rates of SA CCD neurons and evoked discharges in more silent-CCD than control neurons. IS slightly depolarized the resting membrane potential and decreased the current and voltage thresholds of action potential in both intact and dissociated neurons, although the magnitude of depolarization or decrease in action potential threshold was not significantly different between CCD and control. IS-evoked responses were found in a proportion of neurons in each size category including those with and without nociceptive properties. Inflammatory mediators, by increasing the excitability of DRG somata, may contribute to CCD-induced neuronal hyperexcitability and to hyperalgesia and tactile allodynia.