Nociceptor-specific gene deletion using heterozygous Nav1.8-Cre recombinase mice

被引：197

作者：

Stirling, LC ^{[1
]}

Forlani, G ^{[1
]}

Baker, MD ^{[1
]}

Wood, JN ^{[1
]}

Matthews, EA ^{[1
]}

Dickenson, AH ^{[1
]}

Nassar, MA ^{[1
]}

机构：

[1] UCL, Dept Biol, Mol Nocicept Grp, London WC1E 6BT, England

来源：

PAIN | 2005年 / 113卷 / 1-2期

基金：

英国医学研究理事会;

关键词：

pain; knock-out; Cre-loxP; sodium channel; behaviour;

D O I：

10.1016/j.pain.2004.08.015

中图分类号：

R614 [麻醉学];

学科分类号：

100217 ;

摘要：

Na(v)1.8 is a voltage-gated sodium channel expressed only in a subset of sensory neurons of which more than 85% are nociceptors. In order to delete genes in nociceptive neurons, we generated heterozygous transgenic mice expressing Cre recombinase under the control of the Na(v)1.8 promoter. Functional Cre recombinase expression replicated precisely the expression pattern of Na(v)1.8. Cre expression began at embryonic day 14 in small diameter neurons in dorsal root, trigeminal and nodose ganglia, but was absent in non-neuronal or CNS tissues into adulthood. Sodium channel subtypes were normal in isolated DRG neurons. Pain behaviour in response to mechanical or thermal stimuli, and in acute, inflammatory and neuropathic pain was also normal. These data demonstrate that the heterozygous Na(v)1.8-Cre mouse line is a useful tool to analyse the effects of deleting floxed genes on pain behaviour. (C) 2004 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

引用

页码：27 / 36

页数：10

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