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The stress-response
Published in Herman Staudenmayer, Environmental Illness, 2018
Corticotropin-releasing hormone (CRH) is a hypothalamic peptide widespread throughout the brain but best characterized in the hypothalamus, specifically in the paraventricular nucleus (PVN). In animal studies, exogenous stimulation with CRH has been associated with hypercortisolism, sympathetic activation, and behavioral activation and intense arousal (Sutton et al., 1982). Larger doses of CRH administered directly to the CNS produce effects that can be construed as frankly anxiogenic. This includes hyperresponsiveness to sensory stimuli, assumption of the freeze posture, decreased exploration in unfamiliar environments (avoidance), and enhancement of conditioned fear responses during aversive stimuli (Dunn and Berridge, 1990). In humans, parallel symptoms are defining of post-traumatic stress disorder (FTSD). For example, Vietnam combat veterans with PTSD have been found to have higher concentrations of cerebral spinal fluid CRH (Bremner et al., 1997).
Physical Hazards of Space Exploration and the Biological Bases of Behavioral Health and Performance in Extreme Environments
Published in Lauren Blackwell Landon, Kelley J. Slack, Eduardo Salas, Psychology and Human Performance in Space Programs, 2020
Julia M. Schorn, Peter G. Roma
Negative valence systems are responsible for fear, anxiety, threat, and loss, whereas positive valence systems support reward and reinforcement. Fear and anxiety usually manifest in avoidance behaviors and social withdrawal, with physiological markers of increased heart rate; decreased heart rate variability; and elevated cortisol, epinephrine, and norepinephrine. A major component of the negative valence system is stress. The “fight or flight” response is highly complex, with multiple types of stress mediators, like neurotransmitters (noradrenaline, serotonin) and hormones (corticotropin-releasing hormone [CRH], cortisol, and vasopressin). The hypothalamic–pituitary–adrenal (HPA) axis is central to the stress response. In anticipation of a threat, CRH is released from the hypothalamus to the pituitary gland, which releases adrenocorticotrophic hormone (ACTH), which enters the bloodstream and stimulates the release of cortisol and epinephrine from the adrenal gland. Cortisol returns to the hypothalamus to complete a negative feedback loop, diminishing activation (Pariante & Lightman, 2008). Additionally, during a stressful event, levels of inflammatory and immune molecules are also elevated and there are reduced nerve growth factors such as brain-derived neurotrophic factor (BDNF; Berntson et al., 1997; Dowlati et al., 2010; Howren, Lamkin, & Suls, 2009; Jaggar, Fanibunda, Ghosh, Duman, & Vaidya, 2019; Phillips et al., 1998). The limbic system deep in the brain is critical in modulating these processes. Because the limbic system is a functional concept, the strict definition of the anatomical structures within the limbic system is controversial, but it is usually agreed to include the bed nucleus of the stria terminalus, amygdala, and hippocampus (Lebow & Chen, 2016).
Irritable bowel syndrome and the gut microbiota
Published in Journal of the Royal Society of New Zealand, 2020
Phoebe E. Heenan, Jacqueline I. Keenan, Simone Bayer, Myrthe Simon, Richard B. Gearry
Corticotrophin Releasing Hormone (CRH), a vital mediator of the HPA axis and the stress response, is also thought to have a role in mediating IBS symptoms in the gut via modification of the inflammasome. The inflammasome is a component of the immune system that responds to the presence of pathogens via inflammatory responses, resulting in visceral hypersensitivity and increased GI barrier permeability (Ren et al. 2017). An increase in barrier permeability that exposes the enteric immune system (ENS) to luminal antigens then has the potential to perpetuate a positive feedback loop of inflammation, visceral pain, and altered colonic motility.