Department of Physiology, Faculty of Medicine, University of Toronto, 1 King's College Circle, Toronto, Ontario, Canada.
Mol Pain. 2012 Dec 31;8:90. doi: 10.1186/1744-8069-8-90.
CREB has been reported to be activated by injury and is commonly used as marker for pain-related plasticity changes in somatosensory pathways, including spinal dorsal horn neurons and the anterior cingulate cortex (ACC). However no evidence has been reported to support the direct role of activated CREB in injury-related behavioral sensitization (or allodynia). Here we report that genetic enhancement of CREB-mediated transcription selectively in forebrain areas enhanced behavioral responses to non-noxious stimuli after chronic inflammation (CFA model) or nerve injury. In contrast, behavioral acute responses to peripheral subcutaneous injection of formalin did not show any significant difference. Furthermore, acute pain responses to noxious thermal stimuli were also not affected. Our results thus provide direct evidence that cortical CREB-mediated transcription contributes to behavioral allodynia in animal models of chronic inflammatory or neuropathic pain.
CREB 已被报道可被损伤激活，通常被用作躯体感觉通路（包括脊髓背角神经元和扣带回前部皮质）中与疼痛相关的可塑性变化的标志物。然而，尚无证据支持激活的 CREB 在损伤相关的行为敏化（或痛觉过敏）中具有直接作用。在这里，我们报告说，在大脑前区选择性增强 CREB 介导的转录的遗传增强作用可增强慢性炎症（CFA 模型）或神经损伤后对非伤害性刺激的行为反应。相比之下，对皮下注射福尔马林的外周急性反应没有显示出任何显著差异。此外，对有害热刺激的急性疼痛反应也没有受到影响。因此，我们的研究结果直接证明，皮质 CREB 介导的转录有助于慢性炎症或神经性疼痛动物模型中的行为性痛觉过敏。
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