This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Erdmann, G. Articles by Berger, S. Search for Related Content PubMed PubMed Citation Articles by Erdmann, G. Articles by Berger, S.

Loss of Glucocorticoid Receptor Function in the Pituitary Results in Early Postnatal Lethality

German Cancer Research Center, Division Molecular Biology of the Cell I, 69120 Heidelberg, Germany

Address all correspondence and requests for reprints to: Professor Dr. Günther Schütz, German Cancer Research Center, Division Molecular Biology of the Cell I, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. E-mail: g.schuetz{at}dkfz.de.

Glucocorticoid action in the brain is mediated by the glucocorticoid receptor (GR) and the mineralocorticoid receptor, thereby affecting physiological processes such as neurogenesis, synaptic plasticity, and neuroendocrine control. To examine GR function in the regulation of the hypothalamic-pituitary-adrenal axis, we generated GR mutant mice that are homozygous for a conditional GR allele and heterozygous for a transgene that expresses the Cre recombinase under control of the regulatory elements of the mouse calcium/calmodulin-dependent protein kinase II gene, resulting in Cre-mediated recombination in the brain and pituitary. The GR mutants die about 1 wk after birth and display a fulminant increase in plasma corticosterone as well as a severe histopathological phenotype. To assess in which time frame targeting of the pituitary occurs during embryonic development, we used a transgenic line expressing an inducible CreER^T2 fusion protein under the control of the regulatory elements of the calcium/calmodulin-dependent protein kinase II gene. Cre reporter data show that pituitary targeting occurred during embryonic development at the time when glucocorticoid synthesis starts.

This article has been cited by other articles:

				M. V. Schmidt, V. Sterlemann, K. Wagner, B. Niederleitner, K. Ganea, C. Liebl, J. M. Deussing, S. Berger, G. Schutz, F. Holsboer, et al. Postnatal Glucocorticoid Excess Due to Pituitary Glucocorticoid Receptor Deficiency: Differential Short- and Long-Term Consequences Endocrinology, June 1, 2009; 150(6): 2709 - 2716. [Abstract] [Full Text] [PDF]