scholarly journals Litter characteristics and helping context during early life shape the responsiveness of the stress axis in a wild cooperative breeder

2021 ◽  
Vol 75 (12) ◽  
Author(s):  
Aurélie Cohas ◽  
Coraline Bichet ◽  
Rébecca Garcia ◽  
Sylvia Pardonnet ◽  
Sophie Lardy ◽  
...  
Keyword(s):  
Early Life ◽  
Stress Axis

scholarly journals Minireview: Stress-Related Psychiatric Disorders with Low Cortisol Levels: A Metabolic Hypothesis

Endocrinology ◽  
2011 ◽  
Vol 152 (12) ◽  
pp. 4496-4503 ◽  
Author(s):  
Rachel Yehuda ◽  
Jonathan Seckl
Keyword(s):  
Early Life ◽  
Glucocorticoid Receptors ◽  
Model Systems ◽  
Stress Axis ◽  
Pituitary Insufficiency ◽  
Life Challenges ◽  
Early Life Trauma ◽  
Low Cortisol

Several stress-associated neuropsychiatric disorders, notably posttraumatic stress disorder and chronic pain and fatigue syndromes, paradoxically exhibit somewhat low plasma levels of the stress hormone cortisol. The effects appear greatest in those initially traumatized in early life, implying a degree of developmental programming, perhaps of both lower cortisol and vulnerability to psychopathology. In these conditions, lowered cortisol is not due to any adrenal or pituitary insufficiency. Instead, two processes appear involved. First, there is increased target cell sensitivity to glucocorticoid action, notably negative feedback upon the hypothalamic-pituitary-adrenal (stress) axis. Altered density of the glucocorticoid receptor is inferred, squaring with much preclinical data showing early life challenges can permanently program glucocorticoid receptors in a tissue-specific manner. These effects involve epigenetic mechanisms. Second, early life trauma/starvation induces long-lasting lowering of glucocorticoid catabolism, specifically by 5α-reductase type 1 (predominantly a liver enzyme) and 11β-hydroxysteroid dehydrogenase type 2 (in kidney), an effect also seen in model systems. These changes reflect a plausible early-life adaptation to increase the persistence of active cortisol in liver (to maximize fuel output) and kidney (to increase salt retention) without elevation of circulating levels, thus avoiding their deleterious effects on brain and muscle. Modestly lowered circulating cortisol and increased vulnerability to stress-associated disorders may be the outcome. This notion implies a vulnerable early-life phenotype may be discernable and indicates potential therapy by modest glucocorticoid replacement. Indeed, early clinical trials with cortisol have shown a modicum of promise.

scholarly journals Does epigenetic ‘memory’ of early-life stress predispose to chronic pain in later life? A potential role for the stress regulator FKBP5

2019 ◽  
Vol 374 (1785) ◽  
pp. 20190283 ◽  
Author(s):  
S. M. Géranton
Keyword(s):  
Chronic Pain ◽  
Life Stress ◽  
Early Life ◽  
Potential Role ◽  
Adult Life ◽  
Early Life Stress ◽  
Later Life ◽  
Stress Axis ◽  
Evolutionarily Conserved ◽  
Early Life Events

Animal behaviours are affected not only by inherited genes but also by environmental experiences. For example, in both rats and humans, stressful early-life events such as being reared by an inattentive mother can leave a lasting trace and affect later stress response in adult life. This is owing to a chemical trace left on the chromatin attributed to so-called epigenetic mechanisms. Such an epigenetic trace often has consequences, sometimes long-lasting, on the functioning of our genes, thereby allowing individuals to rapidly adapt to a new environment. One gene under such epigenetic control is FKBP5 , the gene that encodes the protein FKPB51, a crucial regulator of the stress axis and a significant driver of chronic pain states. In this article, we will discuss the possibility that exposure to stress could drive the susceptibly to chronic pain via epigenetic modifications of genes within the stress axis such as FKBP5 . The possibility that such modifications, and therefore, the susceptibility to chronic pain, could be transmitted across generations in mammals and whether such mechanisms may be evolutionarily conserved across phyla will also be debated. This article is part of the Theo Murphy meeting issue ‘Evolution of mechanisms and behaviour important for pain’.

scholarly journals Early-life manipulation of cortisol and its receptor alters stress axis programming and social competence

2019 ◽  
Vol 374 (1770) ◽  
pp. 20180119 ◽  
Author(s):  
Maria Reyes-Contreras ◽  
Gaétan Glauser ◽  
Diana J. Rennison ◽  
Barbara Taborsky
Keyword(s):  
Social Competence ◽  
Early Life ◽  
Physiological Mechanism ◽  
Later Life ◽  
Evolutionary Medicine ◽  
Stress Axis ◽  
Long Term Effects ◽  
Coping With Stress ◽  
Expression Of Genes ◽  
Social Challenge

In many vertebrate species, early social experience generates long-term effects on later life social behaviour. These effects are accompanied by persistent modifications in the expression of genes implicated in the stress axis. It is unknown, however, whether stress axis programming can affect the development of social competence, and if so, by which mechanism(s). Here, we used pharmacological manipulations to persistently reprogramme the hypothalamic–pituitary–interrenal axis of juvenile cooperatively breeding cichlids, Neolamprologus pulcher. During the first two months of life, juveniles were repeatedly treated with cortisol, mifepristone or control treatments. Three months after the last manipulation, we tested for treatment effects on (i) social competence, (ii) the expression of genes coding for corticotropin-releasing factor ( crf ), glucocorticoid receptor ( gr1 ) and mineralocorticoid receptor ( mr ) in the telencephalon and hypothalamus and (iii) cortisol levels. Social competence in a social challenge was reduced in cortisol-treated juveniles, which is in accordance with previous work applying early-life manipulations using different social experiences. During early life, both cortisol and mifepristone treatments induced a persistent downregulation of crf and upregulation of mr in the telencephalon. We suggest that these persistent changes in stress gene expression may represent an effective physiological mechanism for coping with stress. This article is part of the theme issue ‘Developing differences: early-life effects and evolutionary medicine’.

scholarly journals Active behaviour during early development shapes glucocorticoid reactivity

2019 ◽  
Author(s):  
Luis A. Castillo-Ramírez ◽  
Soojin Ryu ◽  
Rodrigo J. De Marco
Keyword(s):  
Life Stress ◽  
Early Life ◽  
Developmental Stages ◽  
Early Life Stress ◽  
Later Life ◽  
Stress Axis ◽  
Glucocorticoid Response ◽  
The Central Nervous System ◽  
Response To Stress ◽  
Early Life Events

AbstractGlucocorticoids are the final effectors of the stress axis, with numerous targets in the central nervous system and the periphery. They are essential for adaptation, yet currently it is unclear how early life events program the glucocorticoid response to stress. Here we provide evidence that involuntary swimming at early developmental stages can reconfigure the cortisol response to homotypic and heterotypic stress in larval zebrafish (Danio rerio), also reducing startle reactivity and increasing spontaneous activity as well as energy efficiency during active behaviour. Collectively, these data identify a role of the genetically malleable zebrafish for linking early life stress with glucocorticoid function in later life.

scholarly journals Evolutionary Significance of the Neuroendocrine Stress Axis on Vertebrate Immunity and the Influence of the Microbiome on Early-Life Stress Regulation and Health Outcomes

2021 ◽  
Vol 12 ◽  
Author(s):  
Van A. Ortega ◽  
Emily M. Mercer ◽  
Gerald F. Giesbrecht ◽  
Marie-Claire Arrieta
Keyword(s):  
Stress Response ◽  
Hpa Axis ◽  
Gut Microbiome ◽  
Life Stress ◽  
Early Life ◽  
Biological Response ◽  
Developmental Trajectory ◽  
Stress Axis ◽  
Evolutionary Significance ◽  
Health Maintenance

Stress is broadly defined as the non-specific biological response to changes in homeostatic demands and is mediated by the evolutionarily conserved neuroendocrine networks of the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic nervous system. Activation of these networks results in transient release of glucocorticoids (cortisol) and catecholamines (epinephrine) into circulation, as well as activation of sympathetic fibers innervating end organs. These interventions thus regulate numerous physiological processes, including energy metabolism, cardiovascular physiology, and immunity, thereby adapting to cope with the perceived stressors. The developmental trajectory of the stress-axis is influenced by a number of factors, including the gut microbiome, which is the community of microbes that colonizes the gastrointestinal tract immediately following birth. The gut microbiome communicates with the brain through the production of metabolites and microbially derived signals, which are essential to human stress response network development. Ecological perturbations to the gut microbiome during early life may result in the alteration of signals implicated in developmental programming during this critical window, predisposing individuals to numerous diseases later in life. The vulnerability of stress response networks to maladaptive development has been exemplified through animal models determining a causal role for gut microbial ecosystems in HPA axis activity, stress reactivity, and brain development. In this review, we explore the evolutionary significance of the stress-axis system for health maintenance and review recent findings that connect early-life microbiome disturbances to alterations in the development of stress response networks.

scholarly journals Litter characteristics and helping context during early life shape the responsiveness of the stress axis in a wild cooperative breeder

2021 ◽  
Author(s):  
Aurelie Cohas ◽  
Coraline Bichet ◽  
Rebecca Garcia ◽  
Sylvia Pardonnet ◽  
Sophie Lardy ◽  
...  
Keyword(s):  
Stress Response ◽  
Social Environment ◽  
Hpa Axis ◽  
Stress Responses ◽  
Early Life ◽  
Stress Hormones ◽  
Stress Axis ◽  
Regulatory Processes ◽  
Individual Fitness ◽  
The Social

Stress responses have evolved to quickly and appropriately deal with environmental stressors in order to secure or restore homeostasis. Since the regulation of stress hormones plays a key adaptive role, the regulatory processes controlling stress hormones levels may be under high selective pressure. The social environment during early life (parents and litter characteristics) strongly affects ontogeny of the hypothalamic-pituitary-adrenal (HPA) axis. In cooperative breeders, offspring are also confronted with helpers but whether and how variation in the helping context can affect HPA axis responsiveness of offspring remains unanswered. Combining dexamethasone suppression and adrenocorticotropic hormone stimulation tests, we investigated the link between the social environment and the characteristics of the HPA axis at the early stages of life in wild Alpine marmots. We show that when raised in the presence of helpers, marmot pups exhibit a greater capacity not only to mount, but also to turn off a stress response. The capacity to mount a stress response was also higher as the pups were raised in large litters. Determining impacts of such social modulation of the HPA axis functioning on individual fitness would make an important contribution to our understanding of the evolution of cooperative breeding.

scholarly journals Early-life social environment alters juvenile behavior and neuroendocrine function in a highly social cichlid fish

2018 ◽  
Author(s):  
Tessa K. Solomon-Lane ◽  
Hans A. Hofmann
Keyword(s):  
Early Life ◽  
Cichlid Fish ◽  
Stress Axis ◽  
Social Environments ◽  
Rearing Environment ◽  
Neuroendocrine Function ◽  
Neuroendocrine Mechanisms ◽  
Brain And Behavior ◽  
Juvenile Behavior ◽  
Fitness And Health

AbstractEarly-life experiences can shape adult behavior, with consequences for fitness and health, yet fundamental questions remain unanswered about how early-life social experiences are translated into variation in brain and behavior. The African cichlid fish Astatotilapia burtoni, a model system in social neuroscience, is well known for its highly plastic social phenotypes in adulthood. Here, we rear juveniles in either social groups or pairs to investigate the effects of early-life social environments on behavior and neuroendocrine gene expression. We find that both juvenile behavior and neuroendocrine function are sensitive to early-life effects. Behavior robustly co-varies across multiple contexts (open field, social cue investigation, and dominance behavior assays) to form a behavioral syndrome, with pair-reared juveniles towards the end of syndrome that is less active and socially interactive. Pair-reared juveniles also submit more readily as subordinates. In a separate cohort, we measured whole brain expression of stress and sex hormone genes. Expression of glucocorticoid receptor (GR) 1a was elevated in group-reared juveniles, supporting a highly-conserved role for the stress axis mediating early-life effects. The effect of rearing environment on androgen receptor (AR) α and estrogen receptor (ER) α expression was mediated by treatment duration (1 vs. 5 weeks). Finally, expression of corticotropin-releasing factor (CRF) and GR2 decreased significantly over time. Rearing environment also caused striking differences in gene co-expression, such that expression was tightly integrated in pair-reared juveniles, but not group-reared or isolates. Together, this research demonstrates the important developmental origins of behavioral phenotypes and identifies potential behavioral and neuroendocrine mechanisms.

scholarly journals Stable reprogramming of brain transcription profiles by the early social environment in a cooperatively breeding fish

2013 ◽  
Vol 280 (1753) ◽  
pp. 20122605 ◽  
Author(s):  
Barbara Taborsky ◽  
Linda Tschirren ◽  
Clémence Meunier ◽  
Nadia Aubin-Horth
Keyword(s):  
Early Life ◽  
Social Experience ◽  
Stress Axis ◽  
Expression Ratio ◽  
Transcription Profiles ◽  
Brain Expression ◽  
Cooperatively Breeding ◽  
Hpi Axis ◽  
First Time

Adult social behaviour can be persistently modified by early-life social experience. In rodents, such effects are induced by tactile maternal stimulation resulting in neuroendocrine modifications of the hypothalamic–pituitary–adrenal axis involved in stress responsiveness. Whether similar long-term alterations can occur in the hypothalamic–pituitary–interrenal (HPI) axis of poikilothermic vertebrates is unknown. We compared the expression of four genes of the HPI axis in adults of the cooperatively breeding cichlid Neolamprologus pulcher , which had been exposed to two early-life social treatments 1.5 years prior to brain sampling. Fish reared with parents and siblings had less brain expression of corticotropin-releasing factor and of the functional homologue of the mammalian glucocorticoid receptor (GR1) than individuals reared with same-age siblings only. Expression of the mineralocorticoid receptors (MR) did not differ between treatments, but the MR/GR1 expression ratio was markedly higher in fish reared with parents and siblings. Thus, we show here that early social experience can alter the programming of the stress axis in poikilothermic vertebrates, suggesting that this mechanism is deeply conserved within vertebrates. Moreover, we show for the first time that reprogramming of the stress axis of a vertebrate can be induced without tactile stimulation by parents.

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