Generation of the tamoxifen-inducible DBH-Cre transgenic mouse line DBH-CT

Stubbusch, J.; Majdazari, A.; Schmidt, M.; Schütz, G.; Deller, T.; Rohrer, H.

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Generation of the tamoxifen-inducible DBH-Cre transgenic mouse line DBH-CT

MPG-Autoren

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Stubbusch, J.
Developmental Neurobiology Group, Max Planck Institute for Brain Research, Max Planck Society;

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Majdazari, A.
Developmental Neurobiology Group, Max Planck Institute for Brain Research, Max Planck Society;

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Schmidt, M.
Developmental Neurobiology Group, Max Planck Institute for Brain Research, Max Planck Society;

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Rohrer, H.
Developmental Neurobiology Group, Max Planck Institute for Brain Research, Max Planck Society;

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Zitation

Stubbusch, J., Majdazari, A., Schmidt, M., Schütz, G., Deller, T., & Rohrer, H. (2011). Generation of the tamoxifen-inducible DBH-Cre transgenic mouse line DBH-CT. Genesis, 49(12), 935-941.

Zitierlink: https://hdl.handle.net/11858/00-001M-0000-002E-1D03-5

Zusammenfassung

We generated transgenic mice bearing a tamoxifen-dependent Cre recombinase expressed under the control of the dopamine-beta-hydroxylase promoter. By crossing to the ROSA26 reporter mice we show that tamoxifen-induced Cre recombinase in adult mice specifically activates beta-galactosidase expression in differentiated noradrenergic neurons of the central and peripheral nervous system. Tamoxifen application in adult mice did not induce beta-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. genesis 49:935941, 2011. (c) 2011 Wiley Periodicals, Inc.