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. 2014 Dec;26(12):853-60.
doi: 10.1111/jne.12228.

Modifications of Glucocorticoid Receptors mRNA Expression in the Hypothalamic-Pituitary-Adrenal Axis in Response to Early-Life Stress in Female Japanese Quail

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Free PMC article

Modifications of Glucocorticoid Receptors mRNA Expression in the Hypothalamic-Pituitary-Adrenal Axis in Response to Early-Life Stress in Female Japanese Quail

C Zimmer et al. J Neuroendocrinol. .
Free PMC article

Abstract

Stress exposure during early-life development can programme individual brain and physiology. The hypothalamic-pituitary-adrenal (HPA) axis is one of the primary targets of this programming, which is generally associated with a hyperactive HPA axis, indicative of a reduced negative-feedback. This reduced feedback efficiency usually results from a reduced level of the glucocorticoid receptor (GR) and/or the mineralocorticoid receptor (MR) within the HPA axis. However, a few studies have shown that early-life stress exposure results in an attenuated physiological stress response, suggesting an enhance feedback efficiency. In the present study, we aimed to determine whether early-life stress had long-term consequences on GR and MR levels in quail and whether the effects on the physiological response to acute stress observed in prenatally stressed individuals were underpinned by changes in GR and/or MR levels in one or more HPA axis components. We determined GR and MR mRNA expression in the hippocampus, hypothalamus and pituitary gland in quail exposed to elevated corticosterone during prenatal development, postnatal development, or both, and in control individuals exposed to none of the stressors. We showed that prenatal stress increased the GR:MR ratio in the hippocampus, GR and MR expression in the hypothalamus and GR expression in the pituitary gland. Postnatal stress resulted in a reduced MR expression in the hippocampus. Both early-life treatments permanently affected the expression of both receptor types in HPA axis regions. The effects of prenatal stress are in accordance with a more efficient negative-feedback within the HPA axis and thus can explain the attenuated stress response observed in these birds. Therefore, these changes in receptor density or number as a consequence of early-life stress exposure might be the mechanism that allows an adaptive response to later-life stressful conditions.

Keywords: glucocorticoid receptor; hypothalamic-pituitary-adrenal axis programming; mineralocorticoid receptor; postnatal stress; prenatal stress.

Figures

Fig 1
Fig 1
Mean ± SEM relative gene expression of the mineralocorticoid receptor (white) and glucocorticoid receptor (black) in the hippocampus, hypothalamus and pituitary gland in all females. Different lowercase letters indicate a significant difference between tissues. *Statistically significant difference within tissues.
Fig 2
Fig 2
Mean ± SEM relative expression of the mineralocorticoid receptor (MR) in the hippocampus of quail in the four treatment groups: pre-hatching and post-hatching control (CC), pre-hatching control and post-hatching unpredictable food availability (CF−), pre-hatching corticosterone-treated and post-hatching control (BC) and both treatments (BF−). *Statistically significant difference.
Fig 3
Fig 3
Mean ± SEM glucocorticoid receptor (GR):mineralocorticoid receptor (MR) ratio in the hippocampus of prenatal control (C) and prenatally stressed (B) quail. *Statistically significant difference.
Fig 4
Fig 4
Mean ± SEM relative expression of the mineralocorticoid receptor (MR) in the hypothalamus of prenatal control (C) and prenatally stressed (B) quail. *Statistically significant difference.
Fig 5
Fig 5
Mean ± SEM relative expression of the glucocorticoid receptor (GR) in the hypothalamus of quail in the four treatment group: pre-hatching and post-hatching control (CC), pre-hatching control and post-hatching unpredictable food availability (CF−), pre-hatching corticosterone (CORT)-treated and post-hatching control (BC) and both treatments (BF−). Different lowercase letters indicate significant differences.

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