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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).
Anxiety may be a risk factor for experiencing gastrointestinal symptoms during endurance races: An observational study
Published in European Journal of Sport Science, 2021
Patrick B. Wilson, Hayley Russell, Jamie Pugh
There are a few physiological mechanisms that could explain the observed associations between scores on the psychological scales (particularly STICSA-state scores) and upper GI symptoms (nausea, reflux/regurgitation). Both animal and human experiments have shown that acutely stressful stimuli (that also presumably induce state anxiety) cause the secretion of CRF from the hypothalamus, which results in reduced gastric motility and slowed gastric emptying. (Taché et al., 2001) The exact pathways by which CRF modifies GI function are still being elucidated but likely involve the paraventricular nucleus of the hypothalamus and the dorsal vagal complex nuclei, which influence autonomic nervous system outflow to the GI tract. In humans, delayed gastric emptying has been tied to greater levels of nausea, vomiting, fullness, pain/discomfort, and bloating. (Sarnelli, Caenepeel, Geypens, Janssens, & Tack, 2003), (Khayyam et al., 2010) Another possible mechanism tying state anxiety to upper GI distress is a reduction in splanchnic blood flow, which is a documented phenomenon during prolonged exercise. (ter Steege & Kolkman, 2012) Beyond physical exercise, acute psychological stressors have been shown in some research to impair splanchnic blood flow in humans. (Kuipers, Sauder, Carter, & Ray, 2008)
The interactions of diet-induced obesity and organophosphate flame retardant exposure on energy homeostasis in adult male and female mice
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Gwyndolin M. Vail, Sabrina N. Walley, Ali Yasrebi, Angela Maeng, Kristie M. Conde, Troy A. Roepke
Homeostatic regulation of feeding behaviors and energy balance is a complex system but predominantly controlled via neuroendocrine pathways originating in the hypothalamus (Waye and Trudeau 2011). Briefly, the hypothalamus consists of multiple nuclei in which discrete neuronal subgroups communicate with each other to integrate peripheral indicators of energy states (Williams et al. 2001). With emotional and reward inputs from the limbic forebrain, the hypothalamus synthesizes feeding drive and communicates with the hindbrain for execution (Berthoud 2002; Grill and Hayes 2012). Within the hypothalamus lies the arcuate nucleus (ARC) which sits adjacent to a leaky portion of the blood-brain-barrier, and thus its neurons are in a unique position to directly sense energy state through peripheral signals such as glucose, insulin, leptin, and ghrelin (Saper, Chou, and Elmquist 2002; Schwartz et al. 2000). ARC neurons express receptors for these molecules, and their combined inputs to the paraventricular nucleus (PVN) and lateral hypothalamus (LH) help dictate food intake (Arora and Anubhuti 2006; Nahon 2006). Because hypothalamic control of energy homeostasis is highly regulated through hormone signaling pathways including estrogen receptor (ER) α and peroxisome proliferator-activated receptor (PPAR) γ (Garretson et al. 2015; Mauvais-Jarvis, Clegg, and Hevener 2013; Roepke et al. 2011; Sarruf et al. 2009), any EDC, such as OPFRs, that interact with these receptors may disrupt the complex balance of these pathways, sensitizing the system to metabolic disorders such as obesity and diabetes.
The role of low-level vagus nerve stimulation in cardiac therapy
Published in Expert Review of Medical Devices, 2019
Yuhong Wang, Sunny S. Po, Benjamin J. Scherlag, Lilei Yu, Hong Jiang
The control centers of the autonomic nervous system (ANS) in the brain mainly include the paraventricular nucleus of the hypothalamus (PVN), nucleus tractus solitarius (NTS) and dorsal motor nucleus (DMN). The PVN is a key integrative center for sympathetic tone in the brain and contains two different types of neurons, sympathoexcitatory and sympathoinhibitory [8,9]. Other regional nuclei project to these neurons and alter the activity of the PVN pathways, ultimately influencing the sympathetic outflow to the periphery. Vagal afferent fibers carrying sensory information from the periphery converge on the NTS, whereas vagal efferent fibers originate in the DMN, which provides the vagal output from the brain to the periphery. The neuronal interaction between the NTS and DMN is modulated by many inputs from other relevant nuclei.