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Thermoregulation in the Presence of Microwave Fields
Published in Charles Polk, Elliot Postow, CRC Handbook of Biological Effects of Electromagnetic Fields, 2019
Many CNS sites have been explored with microelectrodes in experimental animals to reveal the existence of single units whose firing rates depend upon the temperature of the tissue in which they are located.33-35 In these experiments, local tissue temperature is controlled with implanted thermodes.36 The activity patterns of CNS thermal sensors resemble those of the skin sensors in many respects. CNS sites that exhibit such thermosensitivity include the medial preoptic area of the hypothalamus, lateral hypothalamus, midbrain reticular formation, medulla, motor cortex, thalamus, spinal cord, and deep viscera.37-40 Many preoptic cells respond to temperature changes in the skin, the spinal cord, and other CNS thermosensitive sites as well as in their own vicinity.41-43 Many neurophysiologists hold this to be evidence that the preoptic area of the hypothalamus is the site of the central "thermostat" as well as the locus of the "integrator-controller". Unfortunately, there is still no direct evidence that these thermally responsive neurons are the actual sensors involved with thermoregulation. A further assumption is that the CNS of humans contains thermal sensors in sites analogous to those that have been found in experimental animals. The strongest evidence marshaled for this assumption is the uniformity of the neurophysiological findings between ectotherms and endotherms.44
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
According to Guyton and Hall,14 the regulation of body temperature occurs in the hypothalamus. This area is apparently deregulated in the chemically sensitive and therefore they are usually cold. The anterior portion of the hypothalamus, especially the preoptic area, is concerned with regulation of body temperature. An increase in the temperature of the blood flowing through this area increases the activity of temperature-sensitive neurons, whereas a decrease in temperature decreases their activity. In turn, these neurons control mechanisms for increasing or decreasing body temperature. Chemically sensitive patients noted for vasospasm usually are cold with temperatures running from 96°F to 97.5°F. Some other chemically sensitive patients are always hot.
Circadian System and Diurnal Activity
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
Sleep pressure acts upon a mutually inhibitory interaction between sleep-promoting and arousal-promoting systems. Sleep-promoting neurons localized in the ventrolateral preoptic area and median preoptic nucleus exert gabaergic and galaninergic inhibitory control over arousal-promoting cell groups localized in multiple arousal centres in the upper brainstem and diencephalon (Fuller et al., 2006). Nonrapid eye movement sleep occurs as a consequence of the activation of neurons within the ventrolateral preoptic area and the progressive decrease in the firing rate of aminergic and cholinergic arousal-promoting neurons resulting from increased release of γ-aminobutyric acid (GABA). Both the activation of the neurons and the GABA release increase proportionally with growing sleep depth. After an adequate amount of sleep, wakefulness occurs at a circadian time during the transition from night to day (Fuller et al., 2006). It is the circadian system that determines the timing of sleep propensity and wakefulness and is often defined as the wake-promoting system (Borbély 1982; Borbély and Achermann, 1999). In the absence of the circadian component, after an SCN lesion, sleep will still occur, but it becomes highly fragmented and is expressed as a continuous series of relatively short sleep episodes promoted by the homeostatic drive alone (Cohen and Albers, 1991).
Fatigue: Is it all neurochemistry?
Published in European Journal of Sport Science, 2018
One big advantage of animal research is the ability to use in vivo brain microdialysis. This technique is based on the kinetic dialysis principle. A small microdialysis catheter or probe is inserted in the area of interest. This probe functions as a blood capillary and is connected to inlet and outlet tubing. Its membrane, permeable to water and small solutes, separates two fluid compartments. The membrane is continuously being flushed on one side (inlet) with a solution that lacks the substances of interest, whereas the other side (outlet) is in contact with the extracellular space. This creates a concentration gradient which in turn causes passive diffusion to take place. Brain microdialysis allows to have direct analysis of extracellular neurotransmitters and metabolites from the brain of resting or active animals with only limited tissue trauma (Meeusen & De Meirleir, 1995; Meeusen et al., 2006). Two studies by Hattori, Li, Matsui, and Nishino (1993) and Hattori, Naoi, and Nishino (1994) – using in vivo brain microdialysis – showed that only 20 min of running on a treadmill significantly increased DA concentration in the rat striatum. Hasegawa, Yazawa, Yasumatsu, Otokawa, and Aihara (2000) measured the neurotransmitter concentrations in the preoptic area and anterior hypothalamus (PO/AH) – the thermoregulatory centre of the brain – in exercising rats, using an in vivo microdialysis technique. They reported that the extracellular level of DOPAC and HVA, both DA metabolites, in the PO/AH increased during treadmill exercise, whereas the levels of serotonin and 5-HIAA were left unchanged. Hasegawa et al. (2000) concluded that DA is the prime candidate for thermoregulatory substances working in the PO/AH.
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.