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Control of the Upper Airway during Sleep
Published in Susmita Chowdhuri, M Safwan Badr, James A Rowley, Control of Breathing during Sleep, 2022
The second REM sleep-related group comprises the cells located in the posterior lateral hypothalamus that synthesize melanin-concentrating hormone (MCH) (156). MCH cells have extensive axonal projections that extend to the pontomedullary reticular formation but their specific targets need studies (157). Although MCH is their unique neurochemical marker, they also use GABA as their transmitter (158). Thus, their enhanced activity during REM sleep would inhibit their postsynaptic targets. Another GABAergic group of REM sleep-active cells is located in a small subregion of the anterior hypothalamus called the extended ventrolateral preoptic nucleus (eVLPO). These cells facilitate the generation of REM sleep through their extensive ascending and descending projections (159).
Physiology of Obesity
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Two groups of neurons in the arcuate nuclei of the hypothalamus can stimulate or inhibit feeding and energy expenditure: (i) pro-opiomelanocortin (POMC) neurons which produce α-melanocyte stimulating hormone and cocaine-amphetamine regulated transcripts (CART) and (ii) neurons that produce neuropeptide Y (NPY) and agouti-related protein (AGRP). Activation of NPY and AGRP neurons increase appetite and feeding and decrease energy expenditure (orexigenic), whereas activation of POMC neurons decrease appetite and feeding and increase energy expenditure leading to reduced energy stores (anorexigenic). NPY, AGRP, ghrelin, melanin-concentrating hormone, glutamate, γ-aminobutyric acid, cortisol, endocannabinoids, endorphins, galanin and orexins A and B are the neurotransmitters that increase appetite and feeding (orexigenic), whereas Leptin, α-melanocyte stimulating hormone, cholecystokinin (CCK), serotonin, norepinephrine, insulin, glucagon-like peptide 1, peptide YY, corticotropin-releasing hormone and CART have a role in satiety. The amygdala (in the limbic system) and prefrontal cortex play an important role in the control of appetite and their activities are coupled with those of the hypothalamus.
The melanocyte and melaninogenesis
Published in Dimitris Rigopoulos, Alexander C. Katoulis, Hyperpigmentation, 2017
Dimitrios Xekardakis, Sabine Krueger-Krasagakis, Konstantinos Krasagakis
Several inhibitors of melanin formation have been reported, such as para-aminobenzoic acid (PABA), quinolines, and benzopyrone.40 Melaninogenesis is also inhibited by hormonal inhibitors and their receptors. These inhibitors include melanocortin’s antagonists, growth factor cytokines and their receptors, G protein–coupled receptors, and other negative regulators. Melanocortin’s antagonists are the melanin-concentrating hormone, the Agouti protein, and the Agouti modifiers. The growth factor cytokines that inhibit melaninogenesis are IL-1, IL-6, interferon (IFN)-α, and IFN-γ and their receptors, and tumor necrosis factor (TNF)-α, TNF-β, and transforming growth factor (TGF)-β1 and their receptors. The G protein–coupled receptors are serotonin, melatonin, dopamine, and acetylocholine and their receptors. Other known negative regulators are the thyroid gland hormones and vitamin E.12 Epidermal growth factor (EGF) and tranexamic acid diminish laser-induced melaninogenesis. Although the mechanism of diminution of melaninogenesis by EGF is not known yet, tranexamic acid reduces melanin contents and tyrosinase activity.41,42 Pleiotrophin (a secreted heparin-binding protein) inhibits melaninogenesis through MITF degradation via the Erk1/2 activation in melanocytes.43 Finally, proton pump inhibitors (PPIs) seem to inhibit melanin biosynthesis via the downregulation of melaninogenesis-associated genes.44
EEG coherence and power spectra during REM sleep related to melatonin intake in mild-to-moderate Alzheimer’s disease: a pilot study
Published in International Journal of Neuroscience, 2023
Manuel Alejandro Cruz-Aguilar, Ignacio Ramírez-Salado, Marisela Hernández-González, Miguel Angel Guevara, Ana Paula Rivera-García
To the best of our knowledge, this is the first study to analyze the effect of melatonin on EEG activity specifically during REM sleep onset in AD patients. In general, we observed that melatonin decreased the RP and EEG coherences of fast frequencies and was associated with a reduction in REM sleep latency. These findings confirm our hypotheses. As in a previous study [36], in this work we found that after melatonin administration a reduction of REM sleep latency occurs in AD patients that approaches the values reported in non-dementia geriatric patients [37, 52]. There is evidence that REM sleep timing is controlled by the activity of GABAergic neurons in the ventrolateral periaqueductal gray and dorsal para-giganto-cellular reticular nucleus, as well as melanin-concentrating hormone neurons in the hypothalamus and cholinergic cells in the PPT and LDT [24]. Thus, our results could suggest that, even in patients with mild-to-moderate AD, the GABAergic neurons involved in REM sleep timing, mainly the hypothalamic pathways, are capable of reacting to the cascade of events that melatonin triggers to facilitate REM sleep installation.
Mechanistically acting anti-obesity compositions/formulations of natural origin: a patent review (2010–2021)
Published in Expert Opinion on Therapeutic Patents, 2022
Pracheta Sengupta, Niyati Tiwari, Tanya Bhatt, Atish T. Paul
The nucleus of the hypothalamus can also be directly influenced by circulating factors as it is partially outside the blood–brain barrier. There are two well-characterized neuronal populations involved in this pathway, namely, appetite inhibiting and appetite-stimulating neurons. The appetite inhibiting neurons further includes proopiomelanocortin (POMC) & cocaine and amphetamine-regulated transcript (CART) co-expressing neurons. Appetite-stimulating neurons includes neuropeptide Y (NPY) and agouti-related peptide co-expressing neurons [24–26]. One of the major genes associated with anorexigenic signaling is the melanocortin receptor genes (MC2R, MC3R, and MC4R) that stimulates melanocortin stimulating hormone (MSH) and melanin-concentrating hormone (MCH) [27]. In the hypothalamus, the neurotransmitter α-melanocyte stimulating hormone (α-MSH) is produced that act on the melanocortin receptor in another part of the hypothalamus to reduce food intake. Lack of leptin on the leptin receptor, in both animals and humans, leads to obesity (Figure 1(C)).
Neurobehavioral and neuroendocrine regulation of energy homeostasis
Published in Postgraduate Medicine, 2019
Stavroula A. Paschou, Konstantinos I. Tsamis, Christina Kanaka-Gantenbein, Elizabeth O. Johnson, George P. Chrousos
During fasting, gastric cells release ghrelin that stimulates the NPY/AgRP neurons. In turn, these neurons activate other ones in the lateral and perifornical hypothalamic areas, which contain orexins and melanin-concentrating hormone (MCH), while they inhibit oxytocin release from paraventricular (PVN) nuclei, in order to evoke acute feeding [2,5]. Ghrelin also provides orexigenic signals to the brainstem via the area postrema [5]. In postprandial state, various hormonal changes occur and favor satiety. After insulin secretion by β pancreatic cells, leptin release by adipocytes and incretins secretion (including glucagon-like peptide 1, GLP-1) by intestine cells, these hormones are conveyed into the ARC, where they activate CART/POMC neurons [2,6]. α-Melanocyte-stimulating hormone (α-MSH) is then released and binded to melanocortin receptors in other hypothalamic regions. These lead to acute hypophagic phenomena, as well as increased energy expenditure [3].