1 Department of Biology, College of Arts and Sciences, Center for Excellence in the Neurosciences, University of New England, Biddeford, ME, USA.
Mol Pain. 2018 Jan-Dec;14:1744806918802703. doi: 10.1177/1744806918802703.
Background Chronic pain affects millions of people worldwide; however, its cellular and molecular mechanisms have not been completely elucidated. It is thought that chronic pain is triggered by nociceptive sensitization, which produces elevated nocifensive responses. A model has been developed in Drosophila melanogaster to investigate the underlying mechanisms of chronic pain using ultraviolet-induced tissue injury to trigger thermal allodynia, a nociceptive hypersensitivity to a normally innocuous stimulus. Larvae were assayed for their behavioral latencies to produce a distinct avoidance response under different thermal conditions. Previously, Decapentaplegic, a member of the Bone Morphogenetic Protein (BMP) family and orthologous to mammalian BMP2/4, was shown to be necessary for the induction of allodynia. Here, we further investigate the BMP pathway to identify other essential molecules necessary to activate the nociceptive sensitization pathway. Results Using the GAL4-UAS-RNAi system to induce a cell-specific knockdown of gene expression, we further explored BMP pathway components to identify other key players in the induction of nociceptive sensitization by comparing the responses of manipulated animals to those of controls. Here, we show that a second BMP, Glass Bottom Boat, and its receptor Wishful Thinking are both necessary for injury-induced thermal allodynia since the formation of sensitization was found to be severely attenuated when either of these components was suppressed. The effects on pain perception appear to be specific to the sensitization system, as the ability to respond to a normally noxious stimulus in the absence of injury was left intact, and no nociceptor morphological defects were observed. Conclusion These results provide further support of the hypothesis that the BMP pathway plays a crucial role in the development of nociceptive sensitization. Because of its strong conservation between invertebrates and mammals, the BMP pathway may be worthy of future investigation for the development of targeted treatments to alleviate chronic pain.
慢性疼痛影响着全球数百万人;然而,其细胞和分子机制尚未完全阐明。人们认为慢性疼痛是由伤害感受性敏化触发的,这会产生升高的伤害感受性反应。已经在黑腹果蝇中开发了一种模型,通过紫外线诱导的组织损伤来触发热性痛觉过敏(对通常无害刺激的伤害感受性过敏),以研究慢性疼痛的潜在机制。幼虫在不同的热条件下进行行为潜伏期测定,以产生明显的回避反应。以前,骨形态发生蛋白(BMP)家族的成员 Decapentaplegic(与哺乳动物 BMP2/4 同源)被证明对痛觉过敏的诱导是必需的。在这里,我们进一步研究了 BMP 途径,以确定激活伤害感受性敏化途径所需的其他必需分子。
使用 GAL4-UAS-RNAi 系统诱导基因表达的细胞特异性敲低,我们进一步探索了 BMP 途径成分,以通过比较操纵动物的反应与对照的反应来确定伤害感受性敏化诱导中的其他关键参与者。在这里,我们表明,第二种 BMP Glass Bottom Boat 及其受体 Wishful Thinking 对于损伤诱导的热性痛觉过敏都是必需的,因为当抑制这些成分中的任何一个时,敏化的形成都被严重减弱。对疼痛感知的影响似乎是特异性的敏化系统,因为在没有损伤的情况下对正常有害刺激的反应能力完好无损,并且没有观察到伤害感受器形态缺陷。
这些结果进一步支持了 BMP 途径在伤害感受性敏化发展中起关键作用的假说。由于其在无脊椎动物和哺乳动物之间的强保守性,BMP 途径可能值得进一步研究,以开发靶向治疗方法来缓解慢性疼痛。