Agarwal Nitin, Offermanns Stefan, Kuner Rohini
Department of Molecular Pharmacology, Pharmacology Institute, University of Heidelberg, Heidelberg, Germany.
Genesis. 2004 Mar;38(3):122-9. doi: 10.1002/gene.20010.
The use of Cre-loxP technology for conditional mutagenesis in pain pathways had been restricted by the unavailability of mice expressing Cre recombinase selectively in functionally distinct components of the nociceptive system. Here we describe the generation of transgenic mouse lines which express Cre recombinase selectively in sensory ganglia using promoter elements of the Na(v)1.8 gene (Scn10a). Cre-mediated recombination was greatly evident in all nociceptive and thermoreceptive neurons of the dorsal root ganglia and trigeminal ganglia, but only in a small proportion of proprioceptive neurons. Cre-mediated recombination was not detectable in the brain, spinal cord, or any nonneural tissues and began perinatally after invasion of primary afferents into the developing spinal cord. Thus, these mice enable selective deletion of genes in subsets of sensory neurons and offer a wide scope for studying potential functions of genes in pain perception, independent of secondary effects arising from developmental defects or global gene ablation.
Cre-loxP技术在疼痛通路中的条件性诱变应用，一直受到无法在伤害感受系统功能不同的组分中选择性表达Cre重组酶的小鼠的限制。在此，我们描述了利用Na(v)1.8基因（Scn10a）的启动子元件，在感觉神经节中选择性表达Cre重组酶的转基因小鼠品系的产生。Cre介导的重组在背根神经节和三叉神经节的所有伤害感受性和温度感受性神经元中非常明显，但仅在一小部分本体感受性神经元中存在。在脑、脊髓或任何非神经组织中未检测到Cre介导的重组，且在初级传入神经侵入发育中的脊髓后围产期开始出现。因此，这些小鼠能够选择性地删除感觉神经元亚群中的基因，并为研究基因在疼痛感知中的潜在功能提供了广阔的空间，而不受发育缺陷或全局基因敲除产生的继发效应的影响。
