scholarly journals The effects of predator odors on stress response and reproduction in Norway rats: A review

2020 ◽  
Vol 10 (4) ◽  
pp. 48-55
Author(s):  
M.A. Kliuchnikova ◽  
P.V. Struchkov ◽  
I.G. Kvasha
Keyword(s):  
Stress Response ◽  
Hpa Axis ◽  
Domestic Cat ◽  
Laboratory Model ◽  
Environmental Harm ◽  
Special Focus ◽  
Pest Species ◽  
Predator Odors ◽  
Potential Predator ◽  
Norway Rats

Norway rat (Rattus norvegicus) is an invaluable laboratory model organism as well as one of the most common rodent pest species. The currently used rodenticides have several significant drawbacks: toxicity to humans and non-target species, environmental harm, the development of avoidance reactions and genetic resistance to the applied substances in rat populations. One of the proposed approaches for rodent pest control is based on natural ways, such as predation, which could be emulated by predator scents. In rodents, olfaction plays a key role in danger recognition, especially in detection of potential predator. Predator odors can activate the hypothalamic-pituitary-adrenal (HPA) axis via central nervous system and thus induce the release of stress hormones. A well-documented suppression of reproduction under psychosocial stress appears to be associated with specific interactions of HPA axis and hypothalamus-pituitary-gonadal (HPG) axis. Hereby we review research on the influences of predator chemical cues on stress response and reproduction in Norway rats with a special focus on long lasting and chronic effects. We describe the effects of predator odors of fox (Vulpes vulpes), ferret (Mustela putorius) and domestic cat (Felis catus) in detail. Assessment of reproductive success in rats may be treated as a robust experimental model to evaluate ecologically relevant stress effects of predator odors. Application of this approach could promote development of environmentally friendly methods to control rat population density.

scholarly journals The impact of bZIP Atf1ortholog global regulators in fungi

2021 ◽  
Author(s):  
Éva Leiter ◽  
Tamás Emri ◽  
Klaudia Pákozdi ◽  
László Hornok ◽  
István Pócsi
Keyword(s):  
Transcription Factors ◽  
Stress Response ◽  
Secondary Metabolite ◽  
Plant Pathogens ◽  
Leucine Zipper ◽  
Secondary Metabolite Production ◽  
Special Focus ◽  
Human Pathogens ◽  
Metabolite Production ◽  
The Impact

Abstract Regulation of signal transduction pathways is crucial for the maintenance of cellular homeostasis and organismal development in fungi. Transcription factors are key elements of this regulatory network. The basic-region leucine zipper (bZIP) domain of the bZIP-type transcription factors is responsible for DNA binding while their leucine zipper structural motifs are suitable for dimerization with each other facilitiating the formation of homodimeric or heterodimeric bZIP proteins. This review highlights recent knowledge on the function of fungal orthologs of the Schizosaccharomyces pombe Atf1, Aspergillus nidulans AtfA, and Fusarium verticillioides FvAtfA, bZIP-type transcription factors with a special focus on pathogenic species. We demonstrate that fungal Atf1-AtfA-FvAtfA orthologs play an important role in vegetative growth, sexual and asexual development, stress response, secondary metabolite production, and virulence both in human pathogens, including Aspergillus fumigatus, Mucor circinelloides, Penicillium marneffei, and Cryptococcus neoformans and plant pathogens, like Fusarium ssp., Magnaporthe oryzae, Claviceps purpurea, Botrytis cinerea, and Verticillium dahliae. Key points • Atf1 orthologs play crucial role in the growth and development of fungi. • Atf1 orthologs orchestrate environmental stress response of fungi. • Secondary metabolite production and virulence are coordinated by Atf1 orthologs.

scholarly journals The co-chaperone Fkbp5 shapes the acute stress response in the paraventricular nucleus of the hypothalamus of male mice

2021 ◽  
Author(s):  
Alexander S. Häusl ◽  
Lea M. Brix ◽  
Jakob Hartmann ◽  
Max L. Pöhlmann ◽  
Juan-Pablo Lopez ◽  
...  
Keyword(s):  
Stress Response ◽  
Hpa Axis ◽  
Paraventricular Nucleus ◽  
Acute Stress ◽  
Negative Regulator ◽  
Neuron Activity ◽  
Cell Type ◽  
Specific Expression ◽  
Acute Stress Response ◽  
Cell Type Specific

AbstractDisturbed activation or regulation of the stress response through the hypothalamic-pituitary-adrenal (HPA) axis is a fundamental component of multiple stress-related diseases, including psychiatric, metabolic, and immune disorders. The FK506 binding protein 51 (FKBP5) is a negative regulator of the glucocorticoid receptor (GR), the main driver of HPA axis regulation, and FKBP5 polymorphisms have been repeatedly linked to stress-related disorders in humans. However, the specific role of Fkbp5 in the paraventricular nucleus of the hypothalamus (PVN) in shaping HPA axis (re)activity remains to be elucidated. We here demonstrate that the deletion of Fkbp5 in Sim1+ neurons dampens the acute stress response and increases GR sensitivity. In contrast, Fkbp5 overexpression in the PVN results in a chronic HPA axis over-activation, and a PVN-specific rescue of Fkbp5 expression in full Fkbp5 KO mice normalizes the HPA axis phenotype. Single-cell RNA sequencing revealed the cell-type-specific expression pattern of Fkbp5 in the PVN and showed that Fkbp5 expression is specifically upregulated in Crh+ neurons after stress. Finally, Crh-specific Fkbp5 overexpression alters Crh neuron activity, but only partially recapitulates the PVN-specific Fkbp5 overexpression phenotype. Together, the data establish the central and cell-type-specific importance of Fkbp5 in the PVN in shaping HPA axis regulation and the acute stress response.

The stress response HPA-axis hormone, glucocorticoid, reduces cellular SKA complex gene expression

2018 ◽  
Vol 260 ◽  
pp. 428-431
Author(s):  
Jingjie Zhao ◽  
Ping Zhang ◽  
Zheng He ◽  
Shuxing Chen ◽  
Teresa Golden ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stress Response ◽  
Hpa Axis

scholarly journals Causal effects of the early caregiving environment on development of stress response systems in children

2015 ◽  
Vol 112 (18) ◽  
pp. 5637-5642 ◽  
Author(s):  
Katie A. McLaughlin ◽  
Margaret A. Sheridan ◽  
Florin Tibu ◽  
Nathan A. Fox ◽  
Charles H. Zeanah ◽  
...  
Keyword(s):  
Nervous System ◽  
Foster Care ◽  
Stress Response ◽  
Hpa Axis ◽  
Stress Responses ◽  
Early Life ◽  
Sensitive Period ◽  
Typically Developing ◽  
Response System ◽  
Stress Response System

Disruptions in stress response system functioning are thought to be a central mechanism by which exposure to adverse early-life environments influences human development. Although early-life adversity results in hyperreactivity of the sympathetic nervous system (SNS) and hypothalamic–pituitary–adrenal (HPA) axis in rodents, evidence from human studies is inconsistent. We present results from the Bucharest Early Intervention Project examining whether randomized placement into a family caregiving environment alters development of the autonomic nervous system and HPA axis in children exposed to early-life deprivation associated with institutional rearing. Electrocardiogram, impedance cardiograph, and neuroendocrine data were collected during laboratory-based challenge tasks from children (mean age = 12.9 y) raised in deprived institutional settings in Romania randomized to a high-quality foster care intervention (n = 48) or to remain in care as usual (n = 43) and a sample of typically developing Romanian children (n = 47). Children who remained in institutional care exhibited significantly blunted SNS and HPA axis responses to psychosocial stress compared with children randomized to foster care, whose stress responses approximated those of typically developing children. Intervention effects were evident for cortisol and parasympathetic nervous system reactivity only among children placed in foster care before age 24 and 18 months, respectively, providing experimental evidence of a sensitive period in humans during which the environment is particularly likely to alter stress response system development. We provide evidence for a causal link between the early caregiving environment and stress response system reactivity in humans with effects that differ markedly from those observed in rodent models.

Limbic Pathways to Stress Control

2016 ◽  
Author(s):  
James P. Herman
Keyword(s):  
Neural Networks ◽  
Prefrontal Cortex ◽  
Stress Response ◽  
Hpa Axis ◽  
Stress Responses ◽  
Physiological Stress ◽  
Brain Regions ◽  
Subcortical Structures ◽  
Stress Control ◽  
Stress Activation

Appropriate control of the HPA (hypothalamo-pituitary-adrenocortical axis) is required for adaptation to physiological and environmental challenges. Inadequate control is linked to numerous stress-related pathologies, including PTSD, highlighting its importance in linking physiological stress responses with behavioral coping strategies. This chapter highlights neurocircuit mechanisms underlying HPA axis adaptation and pathology. Control of the HPA stress response is mediated by the coordinated activity of numerous limbic brain regions, including the prefrontal cortex, hippocampus, and amygdala. In general, hippocampal output inhibits anticipatory HPA axis responses, whereas amygdala subnuclei participate in stress activation. The prefrontal cortex plays an important role in inhibition of context-dependent stress responses. These regions converge on subcortical structures that relay information to paraventricular nucleus corticotropin-releasing hormone neurons, controlling the magnitude and duration of HPA axis stress responses. The output of these neural networks determines the net effect on glucocorticoid secretion, both within the normal adaptive range and in pathological circumstances.

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.

Asymmetry of salivary cortisol and α-amylase responses to psychosocial stress in anorexia nervosa but not in bulimia nervosa

2011 ◽  
Vol 41 (9) ◽  
pp. 1963-1969 ◽  
Author(s):  
P. Monteleone ◽  
P. Scognamiglio ◽  
B. Canestrelli ◽  
I. Serino ◽  
A. M. Monteleone ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Stress Response ◽  
Bulimia Nervosa ◽  
Hpa Axis ◽  
Salivary Cortisol ◽  
Social Stress ◽  
Stress Test ◽  
Trier Social Stress Test ◽  
Enzyme Linked Immunosorbent Assay ◽  
First Time

BackgroundThe stress response involves the activation of the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system (SNS). As a role for stress in determining of the onset and the natural course of eating disorders (EDs) has been proposed, the study of the psychobiology of the stress response in patients with anorexia nervosa (AN) and bulimia nervosa (BN) should be helpful in understanding the pathophysiology of these disorders. The two neurobiological components of the stress response can be easily explored in humans by the measurement of salivary cortisol and α-amylase response to a stressor. Therefore, we assessed salivary cortisol and α-amylase responses to the Trier Social Stress Test (TSST) in symptomatic patients with AN and BN compared to healthy controls.MethodSeven AN women, eight BN women and eight age-matched healthy females underwent the TSST between 1530 and 1700 h. Salivary cortisol and α-amylase levels were measured by an enzyme-linked immunosorbent assay (ELISA).ResultsCompared to healthy women, AN patients showed a normal cortisol response to the TSST, although this occurred at significantly increased hormone levels, and an almost complete absence of response of α-amylase. BN women, however, exhibited enhanced pre-stress levels of salivary α-amylase but a normal response of the enzyme and cortisol to the TSST.ConclusionsThese findings demonstrate, for the first time, the occurrence of an asymmetry between the HPA axis and SNS components of the stress response in the acute phase of AN but not in BN. The pathophysiological significance of this asymmetry remains to be determined.

STABILITY OF A GENERAL DELAY DIFFERENTIAL MODEL OF THE HYPOTHALAMO-PITUITARY-ADRENOCORTICAL SYSTEM

2006 ◽  
Vol 16 (10) ◽  
pp. 3079-3085 ◽  
Author(s):  
DANKA SAVIĆ ◽  
SMILJANA JELIĆ ◽  
NIKOLA BURIĆ
Keyword(s):  
Mathematical Model ◽  
Stability Analysis ◽  
Stress Response ◽  
Linear Stability ◽  
Hpa Axis ◽  
Linear Stability Analysis ◽  
Asymptotically Stable ◽  
Differential Model ◽  
Delay Differential ◽  
Adrenocortical System

Most of the systems in an organism (human included) function in a regular daily rhythm. Hypothalamo-pituitary-adrenocortical (HPA) axis, although mostly known for its role in stress response, probably has a role in conveying rhythmic signals from the major pacemaker, suprachiazmatic nucleus (SCN), to the periphery. A general qualitative nonphenomenological mathematical model of the HPA axis is constructed and its dynamics is examined using linear stability analysis and Roushe's theorem. The results show that this system is asymptotically stable, i.e. it does not generate circadian oscillations, but only responds to the external pacemaker.

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