Accumulating evidence indicates that the brain natriuretic peptide(BNP) and its receptor (natriuretic peptide receptor, NPR) are widely distributed in a variety of tissues including trigeminal ganglion (TG). Furthermore, recent studies support the involvement of the BNP-NPRA pathway in acute and chronic pain. To investigate the role of this pathway in chronic pain, an infraorbital nerve-chronic constriction injury (ION-CCI) model of trigeminal neuralgia (TN) was produced in the rat. The time-course of changes in mechanical pain threshold was examined. We observed an upregulation of BNP and NPR-A and a downregulation of BKCa mRNA and protein in rats subjected to ION-CCI. Patch clamping experiments in vitro found that BKCa currents were significantly reduced in rats subjected to ION-CCI. BNP increased BKCa currents in ION-CCI rats. These results suggest that BNP and NPRA might serve as endogenous pain relievers in ION-CCI rats. Modulation of the BNP/NPR-A/BKCa channel pathway in TG may be a viable strategy for the treatment of TN.

中文翻译：

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BNP/NPR-A/BKCa 通路在大鼠慢性收缩损伤后三叉神经节中的参与

越来越多的证据表明，脑钠肽（BNP）及其受体（natriuretic peptide receptor，NPR）广泛分布于包括三叉神经节（TG）在内的多种组织中。此外，最近的研究支持 BNP-NPRA 通路参与急性和慢性疼痛。为了研究该通路在慢性疼痛中的作用，在大鼠中制作了三叉神经痛 (TN) 的眶下神经-慢性收缩损伤 (ION-CCI) 模型。检查了机械痛阈变化的时间过程。我们观察到接受 ION-CCI 的大鼠中 BNP 和 NPR-A 的上调以及 BKCa mRNA 和蛋白质的下调。体外膜片钳实验发现，在接受 ION-CCI 的大鼠中，BKCa 电流显着降低。BNP 增加了 ION-CCI 大鼠的 BKCa 电流。这些结果表明 BNP 和 NPRA 可能作为 ION-CCI 大鼠的内源性止痛药。TG 中 BNP/NPR-A/BKCa 通道通路的调节可能是治疗 TN 的可行策略。