scholarly journals Efficacy of negative feedback in the HPA axis predicts recovery from acute challenges

2018 ◽  
Vol 14 (7) ◽  
pp. 20180131 ◽  
Author(s):  
Conor C. Taff ◽  
Cedric Zimmer ◽  
Maren N. Vitousek
Keyword(s):  
Stress Response ◽  
Negative Feedback ◽  
Conceptual Models ◽  
Treatment Frequency ◽  
Novel Technique ◽  
Response System ◽  
Downstream Effects ◽  
Wear And Tear ◽  
Stress Response System ◽  
Population Resilience

The glucocorticoid stress response mediates a suite of physiological and behavioural changes that allow vertebrates to cope with transient stressors. Chronically elevated glucocorticoid levels are known to result in a variety of organismal costs, but relatively little is known about the downstream effects of mounting a series of brief, acute spikes in circulating glucocorticoids. Conceptual models of stress suggest that repeated acute stressors might produce ‘wear-and-tear’ on the stress-response system when encountered in sequence. We used a novel technique to experimentally induce acute corticosterone spikes on either three or six consecutive days in incubating tree swallows. Consistent with the ‘wear-and-tear' hypothesis, we found that (i) a sequence of corticosterone spikes produced cumulative effects on corticosterone regulation, (ii) treatment frequency predicted the severity of consequences, and (iii) individual variation in the ability to terminate the stress response through negative feedback predicted the duration of physiological disruption in the group that experienced the most frequent challenges. Our results illustrate the importance of assessing multiple aspects of the hormonal stress response and have implications for understanding both individual and population resilience to repeated transient stressors.

scholarly journals Molecular mechanisms that enhance synapse stability despite persistent disruption of the spectrin/ankyrin/microtubule cytoskeleton

2009 ◽  
Vol 187 (1) ◽  
pp. 101-117 ◽  
Author(s):  
Catherine M. Massaro ◽  
Jan Pielage ◽  
Graeme W. Davis
Keyword(s):  
Stress Response ◽  
Negative Feedback ◽  
Molecular Mechanisms ◽  
Signaling System ◽  
Microtubule Cytoskeleton ◽  
Jnk Pathway ◽  
Response System ◽  
Endogenous Role ◽  
Stress Response System ◽  
Cytoskeletal Disruption

Loss of spectrin or ankyrin in the presynaptic motoneuron disrupts the synaptic microtubule cytoskeleton and leads to disassembly of the neuromuscular junction (NMJ). Here, we demonstrate that NMJ disassembly after loss of α-spectrin can be suppressed by expression of a WldS transgene, providing evidence for a Wallerian-type degenerative mechanism. We then identify a second signaling system. Enhanced MAPK-JNK-Fos signaling suppresses NMJ disassembly despite loss of presynaptic α-spectrin or ankyrin2-L. This signaling system is activated after an acute cytoskeletal disruption, suggesting an endogenous role during neurological stress. This signaling system also includes delayed, negative feedback via the JNK phosphatase puckered, which inhibits JNK-Fos to allow NMJ disassembly in the presence of persistent cytoskeletal stress. Finally, the MAPK-JNK pathway is not required for baseline NMJ stabilization during normal NMJ growth. We present a model in which signaling via JNK-Fos functions as a stress response system that is transiently activated after cytoskeletal disruption to enhance NMJ stability, and is then shut off allowing NMJ disassembly during persistent cytoskeletal disruption.

The oxidative stress response system

2004 ◽  
pp. 59-76 ◽  
Author(s):  
André Korsloot ◽  
Cornelis A.M. van Gestel ◽  
Nico M. van Straalen
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Response System ◽  
Stress Response System

The Evolutionary Life History Model of Externalizing Personality: Bridging Human and Animal Personality Science to Connect Ultimate and Proximate Mechanisms Underlying Aggressive Dominance, Hostility, and Impulsive Sensation Seeking

2017 ◽  
Vol 21 (4) ◽  
pp. 330-353 ◽  
Author(s):  
Michael P. Hengartner
Keyword(s):  
Life History ◽  
Stress Response ◽  
Sensation Seeking ◽  
Inclusive Fitness ◽  
Interpersonal Behavior ◽  
Life History Strategies ◽  
Proximate Mechanisms ◽  
Response System ◽  
Trade Offs ◽  
Stress Response System

The present work proposes an evolutionary model of externalizing personality that defines variation in this broad psychobiological phenotype resulting from genetic influences and a conditional adaptation to high-risk environments with high extrinsic morbidity-mortality. Due to shared selection pressure, externalizing personality is coadapted to fast life history strategies and maximizes inclusive fitness under adverse environmental conditions by governing the major trade-offs between reproductive versus somatic functions, current versus future reproduction, and mating versus parenting efforts. According to this model, externalizing personality is a regulatory device at the interface between the individual and its environment that is mediated by 2 overlapping psychobiological systems, that is, the attachment and the stress-response system. The attachment system coordinates interpersonal behavior and intimacy in close relationships and the stress-response system regulates the responsivity to environmental challenge and both physiological and behavioral reactions to stress. These proximate mechanisms allow for the integration of neuroendocrinological processes underlying interindividual differences in externalizing personality. Hereinafter I further discuss the model's major implications for personality psychology, psychiatry, and public health policy.

scholarly journals Explaining inconsistent results in cancer quality of life studies: the role of the stress–response system

2008 ◽  
Vol 17 (2) ◽  
pp. 174-181 ◽  
Author(s):  
Harry van de Wiel ◽  
Erwin Geerts ◽  
Josette Hoekstra-Weebers
Keyword(s):  
Quality Of Life ◽  
Stress Response ◽  
Response System ◽  
Stress Response System

scholarly journals The Cpx Stress Response System Potentiates the Fitness and Virulence of Uropathogenic Escherichia coli

2013 ◽  
Vol 81 (5) ◽  
pp. 1450-1459 ◽  
Author(s):  
Irina Debnath ◽  
J. Paul Norton ◽  
Amelia E. Barber ◽  
Elizabeth M. Ott ◽  
Bijaya K. Dhakal ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Stress Response ◽  
Aminoglycoside Antibiotic ◽  
Deletion Mutants ◽  
Content Type ◽  
Response System ◽  
Stress Response System ◽  
Tract Infections ◽  
Auxiliary Factor

ABSTRACTStrains of uropathogenicEscherichia coli(UPEC) are the primary cause of urinary tract infections, representing one of the most widespread and successful groups of pathogens on the planet. To colonize and persist within the urinary tract, UPEC must be able to sense and respond appropriately to environmental stresses, many of which can compromise the bacterial envelope. The Cpx two-component envelope stress response system is comprised of the inner membrane histidine kinase CpxA, the cytosolic response regulator CpxR, and the periplasmic auxiliary factor CpxP. Here, by using deletion mutants along with mouse and zebrafish infection models, we show that the Cpx system is critical to the fitness and virulence of two reference UPEC strains, the cystitis isolate UTI89 and the urosepsis isolate CFT073. Specifically, deletion of thecpxRAoperon impaired the ability of UTI89 to colonize the murine bladder and greatly reduced the virulence of CFT073 during both systemic and localized infections within zebrafish embryos. These defects coincided with diminished host cell invasion by UTI89 and increased sensitivity of both strains to complement-mediated killing and the aminoglycoside antibiotic amikacin. Results obtained with thecpxPdeletion mutants were more complicated, indicating variable strain-dependent and niche-specific requirements for this well-conserved auxiliary factor.

Sign in / Sign up

Export Citation Format

Share Document