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首页> 美国卫生研究院文献>Frontiers in Cellular Neuroscience >Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain
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Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain

机译：脊髓糖皮质激素受体信号转导对神经性疼痛大鼠抑郁对机械性异常性疼痛和热痛觉过敏的缓解作用

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Although depression-induced altered pain perception has been described in several laboratory and clinical studies, its neurobiological mechanism in the central nervous system (CNS), particularly in the spinal dorsal horn, remains unclear. Therefore, in this study, we aimed to clarify whether nociceptive sensitivity of neuropathic pain is altered in the olfactory bulbectomy (OB) model of depression and whether glucocorticoid receptor (GR), which is involved in the etio-pathologic mechanisms of both major depression and neuropathic pain, contributes to these processes in the spinal dorsal horn of male Sprague-Dawley rats. The results showed that mechanical allodynia and thermal hyperalgesia induced by spinal nerve ligation (SNL) were attenuated in OB-SNL rats with decreased spinal GR expression and nuclear translocation, whereas non-olfactory bulbectomy (NOB)-SNL rats showed increased spinal GR nuclear translocation. In addition, decreased GR nuclear translocation with normal mechanical nociception and hypoalgesia of thermal nociception were observed in OB-Sham rats. Intrathecal injection (i.t.) of GR agonist dexamethasone (Dex; 4 μg/rat/day for 1 week) eliminated the attenuating effect of depression on nociceptive hypersensitivity in OB-SNL rats and aggravated neuropathic pain in NOB-SNL rats, which was associated with the up-regulation of brain-derived neurotrophic factor (BDNF), TrkB and NR2B expression in the spinal dorsal horn. The present study shows that depression attenuates the mechanical allodynia and thermal hyperalgesia of neuropathic pain and suggests that altered spinal GR-BDNF-TrkB signaling may be one of the reasons for depression-induced hypoalgesia.
机译：尽管在一些实验室和临床研究中已经描述了抑郁症引起的疼痛感知改变，但是其在中枢神经系统（CNS），特别是在脊髓背角的神经生物学机制仍不清楚。因此，在这项研究中，我们旨在弄清在抑郁症的嗅球切除术（OB）模型中神经性疼痛的伤害感受敏感性是否发生了改变，以及糖皮质激素受体（GR）是否与主要抑郁症和抑郁症的病因病理机制有关。神经性疼痛在雄性Sprague-Dawley大鼠的脊髓背角中促成这些过程。结果表明，脊髓神经结扎（SNL）引起的机械性异常性疼痛和热痛觉过敏在脊髓GR表达降低和核易位的OB-SNL大鼠中减弱，而非嗅球切除术（NOB）-SNL大鼠显示脊髓GR核易性增加。此外，在OB-Sham大鼠中观察到GR核移位减少，机械伤害感受正常，热伤害感受觉过敏。鞘内注射GR激动剂地塞米松（Dex； 4μg/大鼠/天，共1周）消除了抑郁症对OB-SNL大鼠伤害性超敏反应的减弱作用以及NOB-SNL大鼠神经痛的加剧，这与脊髓背角中脑源性神经营养因子（BDNF），TrkB和NR2B表达的上调。本研究表明，抑郁症减轻了神经性疼痛的机械性异常性疼痛和热痛觉过敏，并提示改变的脊髓GR-BDNF-TrkB信号传导可能是抑郁症引起的痛觉过敏的原因之一。

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