Stubbusch Jutta, Majdazari Afsaneh, Schmidt Mirko, Schütz Günther, Deller Thomas, Rohrer Hermann
Department of Neurochemistry, Research Group Developmental Neurobiology, Max-Planck-Institute for Brain Research, Frankfurt/M, Germany.
Genesis. 2011 Dec;49(12):935-41. doi: 10.1002/dvg.20773. Epub 2011 Aug 16.
We generated transgenic mice bearing a tamoxifen-dependent Cre recombinase expressed under the control of the dopamine-β-hydroxylase promoter. By crossing to the ROSA26 reporter mice we show that tamoxifen-induced Cre recombinase in adult mice specifically activates β-galactosidase expression in differentiated noradrenergic neurons of the central and peripheral nervous system. Tamoxifen application in adult mice did not induce β-galactosidase activity in parasympathetic neurons that transiently express DBH during development. Thus, this transgenic mouse line represents a valuable tool to study gene function in mature noradrenergic neurons by conditional inactivation.
我们构建了转基因小鼠,其携带在多巴胺-β-羟化酶启动子控制下表达的他莫昔芬依赖性Cre重组酶。通过与ROSA26报告基因小鼠杂交,我们发现成年小鼠中他莫昔芬诱导的Cre重组酶特异性激活中枢和外周神经系统中分化的去甲肾上腺素能神经元中的β-半乳糖苷酶表达。在成年小鼠中应用他莫昔芬不会在发育过程中短暂表达DBH的副交感神经元中诱导β-半乳糖苷酶活性。因此,这种转基因小鼠品系是通过条件性失活研究成熟去甲肾上腺素能神经元中基因功能的有价值工具。