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首页> 外文期刊>Life sciences >Role of spinal voltage-dependent calcium channel α2δ-1 subunit in the expression of a neuropathic pain-like state in mice
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Role of spinal voltage-dependent calcium channel α2δ-1 subunit in the expression of a neuropathic pain-like state in mice

机译：脊髓电压依赖性钙通道α2δ-1亚基在小鼠神经性疼痛样状态表达中的作用

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摘要

The present study was undertaken to investigate the role of spinal voltage-dependent calcium channel α2δ-1 subunit in the expression of a neuropathic pain-like state induced by partial sciatic nerve ligation in mice. In cultured spinal neurons, gabapentin (GBP), which displays the inhibitory effect of α2δ-1 subunit, suppressed the extracellular Ca2+ influx induced by KCl, whereas it failed to inhibit the intracellular Ca2+ release induced by inositol-1,4,5-triphosphate. Seven days after sciatic nerve ligation, the protein level of α2δ-1 subunit in the ipsilateral spinal cord was clearly increased compared to that observed in sham-operated mice. In addition, the mRNA level of α2δ-1 subunit was significantly increased in the dorsal root ganglion, but not in the spinal cord, of nerve-ligated mice. Under these conditions, a marked decrease in the latency of paw-withdrawal against a thermal stimulation and tactile stimulation, induced by sciatic nerve ligation was abolished by repeated intrathecal (i.t.) treatment with GBP. Additionally, the persistent reduction in the nociceptive threshold by i.t. treatment with GBP at the early stage of the neuropathic pain-like state was maintained for 7 days even after GBP withdrawal. It is of interest to note that a single i.t. post-injection of GBP showed a marked and transient inhibitory effect on the developed neuropathic pain-like state, whereas repeated i.t. post-treatment with GBP produced a persistent inhibitory effect during the treatment. In conclusion, we propose here that the neuropathic pain-like state with sciatic nerve ligation is associated with the increased level of the α2δ-1 subunit of Ca2+ channels at the sensory nerve terminal in the spinal dorsal horn of mice. Furthermore, the present data provide evidence that the neuropathic pain may be effectively controlled by repeated treatment with GBP at the early stage.
机译：本研究旨在研究脊髓电压依赖性钙通道α2δ-1亚基在小鼠局部坐骨神经结扎所致神经性疼痛样状态的表达中的作用。在培养的脊髓神经元中，具有α2δ-1亚基抑制作用的加巴喷丁（GBP）抑制了KCl诱导的细胞外Ca2 +内流，但未能抑制肌醇1,4,5-三磷酸诱导的细胞内Ca2 +释放。 。与假手术小鼠相比，坐骨神经结扎7天后，同侧脊髓中α2δ-1亚基的蛋白水平明显升高。另外，神经结扎小鼠的背根神经节中α2δ-1亚基的mRNA水平显着增加，但脊髓中没有。在这些条件下，坐骨神经结扎引起的针对热刺激和触觉刺激的缩爪潜伏期的显着减少通过重复的鞘内（i.t.）鞘内注射治疗得以消除。此外，i.t。持续降低伤害性阈值。即使在撤回GBP后，在神经性疼痛样状态的早期用GBP进行的治疗仍可维持7天。值得一提的是GBP注射后对已发展的神经性疼痛样状态表现出明显且短暂的抑制作用，而反复进行i.t。 GBP的后处理在治疗期间产生了持续的抑制作用。总之，我们在这里提出坐骨神经结扎的神经性疼痛样状态与小鼠脊髓背角感觉神经末梢的Ca2 +通道的α2δ-1亚基水平升高有关。此外，目前的数据提供了证据，即在早期通过GBP的重复治疗可以有效控制神经性疼痛。

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