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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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.

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Developmental plasticity and human health.

Patrick Bateson, David Barker, Timothy Clutton-Brock … (2004)

Many plants and animals are capable of developing in a variety of ways, forming characteristics that are well adapted to the environments in which they are likely to live. In adverse circumstances, for example, small size and slow metabolism can facilitate survival, whereas larger size and more rapid metabolism have advantages for reproductive success when resources are more abundant. Often these characteristics are induced in early life or are even set by cues to which their parents or grandparents were exposed. Individuals developmentally adapted to one environment may, however, be at risk when exposed to another when they are older. The biological evidence may be relevant to the understanding of human development and susceptibility to disease. As the nutritional state of many human mothers has improved around the world, the characteristics of their offspring--such as body size and metabolism--have also changed. Responsiveness to their mothers' condition before birth may generally prepare individuals so that they are best suited to the environment forecast by cues available in early life. Paradoxically, however, rapid improvements in nutrition and other environmental conditions may have damaging effects on the health of those people whose parents and grandparents lived in impoverished conditions. A fuller understanding of patterns of human plasticity in response to early nutrition and other environmental factors will have implications for the administration of public health.

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Early growth conditions, phenotypic development and environmental change.

Pat Monaghan (2008)

Phenotypic development is the result of a complex interplay involving the organism's own genetic make-up and the environment it experiences during development. The latter encompasses not just the current environment, but also indirect, and sometimes lagged, components that result from environmental effects on its parents that are transmitted to their developing offspring in various ways and at various stages. These environmental effects can simply constrain development, for example, where poor maternal condition gives rise to poorly provisioned, low-quality offspring. However, it is also possible that environmental circumstances during development shape the offspring phenotype in such a way as to better prepare it for the environmental conditions it is most likely to encounter during its life. Studying the extent to which direct and indirect developmental responses to environmental effects are adaptive requires clear elucidation of hypotheses and careful experimental manipulations. In this paper, I outline how the different paradigms applied in this field relate to each other, the main predictions that they produce and the kinds of experimental data needed to distinguish among competing hypotheses. I focus on birds in particular, but the theories discussed are not taxon specific. Environmental influences on phenotypic development are likely to be mediated, in part at least, by endocrine systems. I examine evidence from mechanistic and functional avian studies and highlight the general areas where we lack key information.

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Brain corticosteroid receptor balance in health and disease.

E. de Kloet, E Vreugdenhil, M. Oitzl … (1998)

In this review, we have described the function of MR and GR in hippocampal neurons. The balance in actions mediated by the two corticosteroid receptor types in these neurons appears critical for neuronal excitability, stress responsiveness, and behavioral adaptation. Dysregulation of this MR/GR balance brings neurons in a vulnerable state with consequences for regulation of the stress response and enhanced vulnerability to disease in genetically predisposed individuals. The following specific inferences can be made on the basis of the currently available facts. 1. Corticosterone binds with high affinity to MRs predominantly localized in limbic brain (hippocampus) and with a 10-fold lower affinity to GRs that are widely distributed in brain. MRs are close to saturated with low basal concentrations of corticosterone, while high corticosterone concentrations during stress occupy both MRs and GRs. 2. The neuronal effects of corticosterone, mediated by MRs and GRs, are long-lasting, site-specific, and conditional. The action depends on cellular context, which is in part determined by other signals that can activate their own transcription factors interacting with MR and GR. These interactions provide an impressive diversity and complexity to corticosteroid modulation of gene expression. 3. Conditions of predominant MR activation, i.e., at the circadian trough at rest, are associated with the maintenance of excitability so that steady excitatory inputs to the hippocampal CA1 area result in considerable excitatory hippocampal output. By contrast, additional GR activation, e.g., after acute stress, generally depresses the CA1 hippocampal output. A similar effect is seen after adrenalectomy, indicating a U-shaped dose-response dependency of these cellular responses after the exposure to corticosterone. 4. Corticosterone through GR blocks the stress-induced HPA activation in hypothalamic CRH neurons and modulates the activity of the excitatory and inhibitory neural inputs to these neurons. Limbic (e.g., hippocampal) MRs mediate the effect of corticosterone on the maintenance of basal HPA activity and are of relevance for the sensitivity or threshold of the central stress response system. How this control occurs is not known, but it probably involves a steady excitatory hippocampal output, which regulates a GABA-ergic inhibitory tone on PVN neurons. Colocalized hippocampal GRs mediate a counteracting (i.e., disinhibitory) influence. Through GRs in ascending aminergic pathways, corticosterone potentiates the effect of stressors and arousal on HPA activation. The functional interaction between these corticosteroid-responsive inputs at the level of the PVN is probably the key to understanding HPA dysregulation associated with stress-related brain disorders. 5. Fine-tuning of HPA regulation occurs through MR- and GR-mediated effects on the processing of information in higher brain structures. Under healthy conditions, hippocampal MRs are involved in processes underlying integration of sensory information, interpretation of environmental information, and execution of appropriate behavioral reactions. Activation of hippocampal GRs facilitates storage of information and promotes elimination of inadequate behavioral responses. These behavioral effects mediated by MR and GR are linked, but how they influence endocrine regulation is not well understood. 6. Dexamethasone preferentially targets the pituitary in the blockade of stress-induced HPA activation. The brain penetration of this synthetic glucocorticoid is hampered by the mdr1a P-glycoprotein in the blood-brain barrier. Administration of moderate amounts of dexamethasone partially depletes the brain of corticosterone, and this has destabilizing consequences for excitability and information processing. 7. The set points of HPA regulation and MR/GR balance are genetically programmed, but can be reset by early life experiences involving mother-infant interaction. 8. (ABSTRACT TRUNCATED)

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Author and article information

Journal

Journal ID (nlm-ta): J Neuroendocrinol

Journal ID (iso-abbrev): J. Neuroendocrinol

Journal ID (publisher-id): jne

Title: Journal of Neuroendocrinology

Publisher: BlackWell Publishing Ltd (Oxford, UK )

ISSN (Print): 0953-8194

ISSN (Electronic): 1365-2826

Publication date (Print): December 2014

Publication date (Electronic): 17 November 2014

Volume: 26

Issue: 12

Pages: 853-860

Affiliations

School of Psychology and Neuroscience, University of St Andrews St Andrews, UK

Author notes

Correspondence to: C. Zimmer, School of Psychology and Neuroscience, University of St Andrews, South Street, St Andrews KY16 9JP, UK (e-mail: cz6@ 123456st-andrews.ac.uk ).

Article

DOI: 10.1111/jne.12228

PMC ID: 4260142

PubMed ID: 25303060

SO-VID: 964a7bd9-eece-46cd-bc94-0b5df81cd5bf

License:

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

History

Date received : 28 July 2014

Date revision received : 01 October 2014

Date accepted : 02 October 2014

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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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Most cited references 54

Developmental plasticity and human health.

Early growth conditions, phenotypic development and environmental change.

Brain corticosteroid receptor balance in health and disease.

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