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Na V 1.8/Na V 1.9 双删除轻微影响小鼠的急性疼痛反应

Marta Alves-Simões¹, Laura Teege², Cecilia Tomni³

¹Molecular Nociception Group, Wolfson Institute for Biomedical Research, University College London, Gower Street, London, United Kingdom.

|October 9, 2024

概括

该研究产生了缺乏NaV1.8和NaV1.9通道的双淘汰赛小鼠,揭示了它们在疼痛信号中的作用,并提供了研究与疼痛相关的遗传变异的工具.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

抗四极毒素 (TTXr) 的电压接通道亚型NaV1.8和NaV1.9对于外围疼痛信号发送至关重要.
这些通道 (由SCN10A和SCN11A编码) 在感知神经元中表达,并因突变而涉及各种人类疼痛疾病.

研究的目的:

为了研究NaV1.8和NaV1.9通道损失的功能影响.
建立一种有价值的工具,用于在本地生理环境中研究NaV1.8和NaV1.9的致病变体.

主要方法:

使用CRISPR/Cas9基因编辑生成NaV1.8/NaV1.9双淘汰赛 (DKO) 的小鼠.
经验证的道淘汰通过背部根质 (DRG) 神经元的全细胞记录.
利用全球RNA测序来分析DKO神经元中的基因表达变化.

主要成果:

证实了DKO DRG神经元中没有NaV1.8和NaV1.9电流.
在DKO神经元中观察到C-LTMR标记基因和疼痛调节神经的放松调节.
在DKO小鼠中仅报告了中度受损的急性疼痛行为,这表明复杂的疼痛调节.

结论:

NaV1.8和NaV1.9通道在疼痛感知中起着重要作用.
DKO鼠标模型是研究个人人类疼痛相关通道变异的功能的一个强大的资源.
进一步的研究可以利用这种模型来了解对疼痛疾病的遗传贡献.

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