Role of glucocorticoid receptor gene in vulnerability for major depression: commentary on Neigh and Nemeroff

2006 ◽  
Vol 17 (10) ◽  
pp. 386 ◽  
Author(s):  
Filip Van Den Eede ◽  
Dirk van West ◽  
Christine Van Broeckhoven ◽  
Stephan J. Claes
Keyword(s):  
Major Depression ◽  
Glucocorticoid Receptor ◽  
Receptor Gene ◽  
Glucocorticoid Receptor Gene

Glucocorticoid Receptor Gene Polymorphisms in Premenopausal Women with Major Depression

2008 ◽  
Vol 40 (3) ◽  
pp. 194-198 ◽  
Author(s):  
P. Krishnamurthy ◽  
P. Romagni ◽  
S. Torvik ◽  
P. Gold ◽  
D. Charney ◽  
...  
Keyword(s):  
Major Depression ◽  
Glucocorticoid Receptor ◽  
Gene Polymorphisms ◽  
Receptor Gene ◽  
Premenopausal Women ◽  
Glucocorticoid Receptor Gene ◽  
Receptor Gene Polymorphisms

The role of the glucocorticoid receptor gene ( NR3C1 ) for the processing of aversive stimuli

2016 ◽  
Vol 107 ◽  
pp. 8-13 ◽  
Author(s):  
Katja Kerstin Schneider ◽  
Christian Frings ◽  
Jobst Meyer ◽  
Andrea B. Schote
Keyword(s):  
Glucocorticoid Receptor ◽  
Receptor Gene ◽  
Aversive Stimuli ◽  
Glucocorticoid Receptor Gene

scholarly journals Glucocorticoid Receptor Gene-Based SNP Analysis in Patients with Recurrent Major Depression

2005 ◽  
Vol 31 (3) ◽  
pp. 620-627 ◽  
Author(s):  
Dirk van West ◽  
Filip Van Den Eede ◽  
Jurgen Del-Favero ◽  
Daniel Souery ◽  
Karl-Fredrik Norrback ◽  
...  
Keyword(s):  
Major Depression ◽  
Glucocorticoid Receptor ◽  
Receptor Gene ◽  
Snp Analysis ◽  
Glucocorticoid Receptor Gene

scholarly journals Conditional Inactivation of Glucocorticoid Receptor Gene in Dopamine-β-Hydroxylase Cells Impairs Chromaffin Cell Survival

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1775-1781 ◽  
Author(s):  
Rosanna Parlato ◽  
Christiane Otto ◽  
Jan Tuckermann ◽  
Stefanie Stotz ◽  
Sylvia Kaden ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Chromaffin Cells ◽  
Chromaffin Cell ◽  
Apoptotic Cell ◽  
Receptor Gene ◽  
Adrenal Chromaffin Cells ◽  
Glucocorticoid Receptor Gene ◽  
Conditional Inactivation ◽  
Adrenal Chromaffin

Glucocorticoid hormones (GCs) have been thought to determine the fate of chromaffin cells from sympathoadrenal progenitor cells. The analysis of mice carrying a germ line deletion of the glucocorticoid receptor (GR) gene has challenged these previous results because the embryonic development of adrenal chromaffin cells is largely unaltered. In the present study, we have analyzed the role of GC-dependent signaling in the postnatal development of adrenal chromaffin cells by conditional inactivation of the GR gene in cells expressing dopamine-β-hydroxylase, an enzyme required for the synthesis of noradrenaline and adrenaline. These mutant mice are viable, allowing to study whether in the absence of GC signaling further development of the adrenal medulla is affected. Our analysis shows that the loss of GR leads not only to the loss of phenylethanolamine-N-methyl-transferase expression and, therefore, to inhibition of adrenaline synthesis, but also to a dramatic reduction in the number of adrenal chromaffin cells. We provide evidence that increased apoptotic cell death is the main consequence of GR loss. These findings define the essential role of GCs for survival of chromaffin cells and underscore the specific requirement of GCs for adrenergic chromaffin cell differentiation and maintenance.

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