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Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Some of the behavioral effects of stimulation are the following: (1) Stimulation in the lateral hypothalamus not only causes thirst and eating, as discussed earlier, but also increases the general level of activity of the animal, sometimes leading to overt rage and fighting as discussed subsequently. (2) Stimulation in the ventromedial nucleus and surrounding areas mainly causes and affects opposite to those caused by lateral hypothalamic stimulation, that is, a sense of satiety, decreased eating, and tranquility. The clinician rarely sees this tranquility in chemically sensitive patients, but it does occur especially after a 3–7-day fast and little toxic exposures, when the nutrition is right and all injections are steady. (3) Stimulation of a thin zone of periventricular nuclei, located immediately adjacent to the third ventricle (or also stimulation of the central gray area of the mesencephalon that is continuous with this portion of the hypothalamus), usually leads to fear and punishment reactions. One frequently observes these tougher reactions in the chemically sensitive upon exposure to excessive molds, and mycotoxins, pesticides or natural gas, or other toxics. (4) Sexual drive can be stimulated from several areas of the hypothalamus, especially the most anterior and most posterior portions of the hypothalamus.
Systematic review on gastric electrical stimulation in obesity treatment
Published in Expert Review of Medical Devices, 2019
Alimujiang Maisiyiti, Jiande Dz Chen
Central neuronal effects: A recent study reported that all three methods of GES (short pulse, long pulse, and trains of short pulses) were able to activate gastric distention-responsive neurons in the paraventricular nucleus. However, in gastric distention-inhibitory neurons (one specific type of neurons), opposite effects were noted between GES using trains of short pulses with different parameters used for treating obesity and gastroparesis [49]. These results suggest possible distinct central mechanisms with different methods of GES. Similar central neuronal effects of GES were also found in the hippocampus and the ventromedial nucleus [15,50].
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
Centrally, there are also many areas of the brain that control fluid balance including the PVH, supraoptic nucleus, median preoptic area, organum vasculosum laminae terminalis, and subfornical organ (Curtis 2009). Many of these nuclei express ERs and are involved in the control of fluid balance in response to E2 (Curtis 2009; Santollo and Daniels 2015a, 2015b; Santollo, Marshall, and Daniels 2013; Shughrue, Lane, and Merchenthaler 1997). In hormone replacement therapies, E2 produced a direct effect on water intake (Krause et al. 2003; Santollo, Marshall, and Daniels 2013), its actions mediated in part through dampening of angiotensin II (AngII) signaling (Danielsen and Buggy 1980; Findlay, Fitzsimons, and Kucharczyk 1979; Jonklaas and Buggy 1984; Kisley et al. 1999). Potentially, OPFRs interfere with this estrogen-sensitive balance leading to changes in fluid intake. However, like any homeostatic function, thirst is regulated through a multitude of pathways, allowing for alternate avenues of OPFR actions. Thirst is closely related to energy homeostasis, and the powerful “hunger” hormone ghrelin is also known to exert effects on fluid intake, reducing water consumption by inhibiting Ang II (Hashimoto et al. 2010; Mietlicki, Nowak, and Daniels 2009; Plyler and Daniels 2017), which as previously indicated, is also under the influence of E2. Conversely, intracerebroventricular infusions of Ang II diminishes food intake and enhances energy expenditure, establishing an Ang II link between food and fluid intake mediated by ghrelin (Porter and Potratz 2004). In our current study, OPFR decreased circulating ghrelin in male mice on LFD, supporting a ghrelin-mediated hypothesis for the dipsogenic effect of OPFR on male mice. Finally, somatostatin, produced both centrally in the ventromedial nucleus of the hypothalamus, and peripherally by delta cells in the digestive system, is involved in thirst generation and may be a target for OPFR dysregulation. Central action of somatostatin increases food and water intake (Karasawa et al. 2014; Stengel et al. 2010), and was shown to be altered by exposure to bisphenol A, another well-known estrogenic EDC (Facciolo et al. 2002, 2005). Taken together, these data offer a precedented route for OPFR EDC action on fluid regulation.