Differential effects of DRN GR deletion in female mice may provide insight into the greater incidence of depression and specific depression symptoms in women.
Additionally, adequate antidepressant treatment may be effective for the remission of depressive symptoms regardless of NR3C1 1 F exon methylation status.
Parents reported on their depressive symptoms, children reported negative mood symptoms, and youths completed blood draws from which expression of Glucocorticoid Receptor (GR) and Beta2 Adrenergic Receptor (β<sub>2</sub>-AR) genes was extracted.
Analyses demonstrated a trend in the association between both maternal trait anxiety and depression symptoms with placental gene expression of NR3C1(adj.β=0.220,p=0.067;adj.β=0.212,p=0.064 respectively).
Findings also indicate that hypermethylation of NR3C1 is linked with a number of negative child outcomes including greater emotional lability-negativity, higher levels of ego undercontrol, more externalizing behavior, and greater depressive symptoms.
Higher placental NR3C1 mRNA partly mediated the association between maternal depressive symptoms during pregnancy and infant regulatory behaviors (p < 0.05).
The aim of this study was to investigate whether single nucleotide polymorphisms (SNPs) in genes of the stress hormone signaling pathway, specifically FKBP5, NR3C1, and CRHR1, are associated with depressive symptoms during and after pregnancy.
Regulation of mRNA expression encoding chaperone and co-chaperone proteins of the glucocorticoid receptor in peripheral blood: association with depressive symptoms during pregnancy.
We examined if single nucleotide polymorphisms (SNPs) and their haplotypes spanning the entire NR3C1 are associated with depressive disorders and with self-reported depressive symptoms in adulthood.
We will review some of the evidence for modulation of the GR by antidepressants and we will provide further insight into how antidepressants may regulate the GR to overcome depressive symptoms.
An association study was performed to determine the relationship between GR gene polymorphisms, childhood adversity, HPA-axis markers and depressive symptoms.