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The Role of Endogenous Sleep-promoting Substances
Published in Clete A. Kushida, Sleep Deprivation, 2004
Ferenc Obal, Fabio Garcia-Garcia, James M. Krueger
A few additional substances are implicated in sleep regulation, although the evidence for their sleep role is substantially less than that of the molecules discussed above. Oleamide is an unsaturated fatty acid that was isolated from the CSF of a sleep-deprived cat (152). Oleamide is structurally related to the endogenous cannabinoid anandamide, and it is possible that oleamide promotes NREM sleep via cannabinoid receptors directly or indirectly by inhibiting anan-damide metabolism (153). Cortistatin is a peptide displaying strong homology with somatostatin. It is an inhibitory neurotransmitter in the cerebral cortex and in the hippocampus (154). Cortistatin seems to promote NREM sleep, but the sleep responses have not been thoroughly studied. Cholecystokinin (CCK) is a peptide hormone released from the duodenum in response to fats and proteins, and might be involved in the mediation of postprandial sleep. CCK promotes NREM sleep (155). The action is peripheral and might be mediated by vagal sensory neurons. Insulin is a peptide hormone released from the pancreas that stimulates glucose uptake by skeletal muscle and adipocytes and has a fundamental role in the regulation of metabolism of sugar, lipid, and protein, and in tissue growth. Promotion of NREM sleep was reported after intracerebroventricular administration of insulin in rats (156). However, the evidence is scarce implicating insulin in sleep regulation, and the sleep-promoting activity of intracerebral insulin might be mediated by IGF-1 receptors (157). Nitric oxide (NO) is also implicated in sleep regulation (158). The findings linking NO to regulation of NREM sleep are controversial (159), whereas the results are consistent that suggest that NO stimulates REM sleep by acting in the pedunculopontine tegmen-tum in the brainstem (160). Interestingly, neural NO synthase knockout mice have less REM sleep whereas inducible NO synthase knockout mice have more REM sleep (161).
In vitro prediction of in vivo pseudo-allergenic response via MRGPRX2
Published in Journal of Immunotoxicology, 2021
Linu M. John, Charlotte M. Dalsgaard, Claus B. Jeppesen, Kilian W. Conde-Frieboes, Katrine Baumann, Niels P. H. Knudsen, Per S. Skov, Birgitte S. Wulff
Sermorelin, Substance P, cetrorelix and icatibant were tested in the DiscoverX β-arrestin assay in order to confirm that compounds reported (Chen et al. 2008; Olivennes et al. 2003; Amatya et al. 2010; Baş et al. 2015; McNeil et al. 2015) to induce skin irritation in humans also activated MRGPRX2. Cortistatin (a somatostatin receptor agonist) - reported to also be a potent agonist at MRGPRX2 - was used as a comparator (Allia et al. 2005; Sieler et al. 2008; Solinski et al. 2014). Cetrorelix was found to be a full agonist (pEC50 = 6.6 nM) at MRGPRX2 with comparable potency to cortistatin (pEC50 = 6.6, Figure 1). In contrast, sermorelin and Substance P displayed lower estimated potencies (pEC50 = 5.0 and 4.8, respectively), and icatibant was inactive (Figure 1).
Serum Cortistatin Levels in Patients with Ocular Active and Ocular Inactive Behçet Disease
Published in Ocular Immunology and Inflammation, 2020
Mehmet Balbaba, Fatih Ulaş, Sevinç Arzu Postacı, Burak Öz, Süleyman Aydın
Cortistatin (CST) is a recently discovered neuropeptide, which is structurally similar to somatostatin. It has been shown that CST shares many pharmacological and functional properties with somatostatin, including the inhibition of neuronal activity and the suppression of growth hormone, prolactin, and insulin secretion.4 However, CST also has many properties that differ from somatostatin, including the induction of slow-wave sleep, reduction of locomotor activity and inhibition of cellular proliferation.4,5 CST is produced by macrophages and T cells in response to inflammatory and immune stimulations and supports a physiological role of CST in the immune system.6 It inhibits the proliferation of Th1 cells and release of proinflammatory cytokines (IL-1, IL-6, IL-12 and IFN-gamma), while increasing the anti-inflammatory signals (IL-10).7