scholarly journals How Truly Conserved Is the “Well-Conserved” Vertebrate Stress Response?

2019 ◽  
Vol 59 (2) ◽  
pp. 273-281 ◽  
Author(s):  
L M Romero ◽  
B M G Gormally
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Stress Response ◽  
Stress Responses ◽  
Species Variation ◽  
Functional Variation ◽  
Fitness Consequences ◽  
Fight Or Flight Response ◽  
Pituitary Adrenal Axis ◽  
Functional Output

Abstract The vertebrate stress response is considered to be a highly conserved suite of responses that are evolved to help animals survive noxious environmental stimuli. The two major pathways of the stress response include the catecholamine release that is part of the autonomic nervous system and comprises the immediate fight-or-flight response, and the slower release of corticosteroids from the hypothalamic–pituitary–adrenal axis that help orchestrate longer-term responses. These two pathways are present in every vertebrate yet examined, and the anatomical and physiological architecture underlying these pathways are consistent. Despite these structural similarities, however, recent data indicate substantial temporal and species variation in the actual regulation of these pathways. For example, activation of both pathways varies seasonally in some species but not others, and responses of both pathways can be extensively modulated by an individual’s previous experience. Consequently, even though the anatomy of the stress response is highly conserved, the activation and functional output is not highly conserved. Given this variation, it is perhaps not surprising that it is proving difficult to correlate individual stress responses with differences in fitness outcomes. This review summarizes the challenge of making broad generalized assumptions about fitness consequences of the stress response given the functional variation we observe.

The Potential Role of a Corticotropin-Releasing Factor Receptor-1 Antagonist in Psychiatric Disorders

CNS Spectrums ◽  
2008 ◽  
Vol 13 (6) ◽  
pp. 467-483 ◽  
Author(s):  
Stephen M. Stahl ◽  
Dana D. Wise
Keyword(s):  
Stress Response ◽  
Psychiatric Disorders ◽  
Stress Responses ◽  
Potential Role ◽  
Corticotropin Releasing Factor ◽  
Recovering Alcoholic ◽  
Mood And Cognition ◽  
Pituitary Adrenal Axis

The hypothalamic-pituitary-adrenal axis is a key mediator of the stress response in humans. The corticotropin-releasing factor (CRF) type 1 receptor (CRFR-1) in the pituitary gland is a gatekeeper for that response, and the CRFR-1 receptor is also present in many other mood- and cognition-related neural structures. Behaviorally, a number of relationships between stress and psychiatric disorders can be observed: chronic or repeated stress is associated with onset of depression; stressors can cause a recovering alcoholic to relapse; overactive stress responses mark many anxiety disorders; and insomnia can arise from an overactive stress response. Thus, a CRFR-1 antagonist could be useful for treating or preventing the consequences of CRF-mediated stress in depression, anxiety, insomnia, and substance abuse.

scholarly journals Plasma Transcortin Influences Endocrine and Behavioral Stress Responses in Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (2) ◽  
pp. 649-659 ◽  
Author(s):  
Elodie M. Richard ◽  
Jean-Christophe Helbling ◽  
Claudine Tridon ◽  
Aline Desmedt ◽  
Amandine M. Minni ◽  
...  
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Learned Helplessness ◽  
Critical Role ◽  
Adaptive Responses ◽  
Adrenal Axis ◽  
Response To Stress ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Deficient Mice ◽  
Pituitary Adrenal Axis

Glucocorticoids are released after hypothalamus-pituitary-adrenal axis stimulation by stress and act both in the periphery and in the brain to bring about adaptive responses that are essential for life. Dysregulation of the stress response can precipitate psychiatric diseases, in particular depression. Recent genetic studies have suggested that the glucocorticoid carrier transcortin, also called corticosteroid-binding globulin (CBG), may have an important role in stress response. We have investigated the effect of partial or total transcortin deficiency using transcortin knockout mice on hypothalamus-pituitary-adrenal axis functioning and regulation as well as on behaviors linked to anxiety and depression traits in animals. We show that CBG deficiency in mice results in markedly reduced total circulating corticosterone at rest and in response to stress. Interestingly, free corticosterone concentrations are normal at rest but present a reduced surge after stress in transcortin-deficient mice. No differences were detected between transcortin-deficient mice for anxiety-related traits. However, transcortin-deficient mice display increased immobility in the forced-swimming test and markedly enhanced learned helplessness after prolonged uncontrollable stress. The latter is associated with an approximately 30% decrease in circulating levels of free corticosterone as well as reduced Egr-1 mRNA expression in hippocampus in CBG-deficient mice. Additionally, transcortin-deficient mice show no sensitization to cocaine-induced locomotor responses, a well described corticosterone-dependent test. Thus, transcortin deficiency leads to insufficient glucocorticoid signaling and altered behavioral responses after stress. These findings uncover the critical role of plasma transcortin in providing an adequate endocrine and behavioral response to stress.

scholarly journals Salivary α-Amylase And Chromogranin A In Anxiety-Related Research

Folia Medica ◽  
2014 ◽  
Vol 56 (4) ◽  
pp. 233-236 ◽  
Author(s):  
Valeria T. Tananska
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Genetic Code ◽  
Chemical Reactions ◽  
Chromogranin A ◽  
Related Research ◽  
Hypothalamic Pituitary Adrenal ◽  
Antifungal Action ◽  
Biochemical Research ◽  
Pituitary Adrenal Axis

Abstract Salivary α-amylase (sAA) and chromogranin A (sCgA) are at the forefront of current biochemical research on anxiety. Their use is being driven by the sudden surge of interest in “salivaomics,” a new field in medicine studying saliva’s genetic code, proteome and methabolom. Interestingly, it is not the primary functions of the enzyme and the protein, but the ingenious capture of their secondary ones (maintenance of the acid-alkaline balance and bactericidal / antifungal action) that allows for a swift, precise and pain-free measurement under physical and mental duress. Upon stimulation, sAA and sCgA are almost simultaneously released. Studying them allows a closer look at the autonomic nervous system (ANS) as opposed to the hypothalamic-pituitary-adrenal axis (HPA), which involves a long cascade of complex, hard to measure and interpret bio-chemical reactions.

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.

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