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      α-Melanophore-Stimulating Hormone (α-MSH) Antagonizes Interleukin-1β-Induced Hyperalgesia and Fos Expression in the Paraventricular and Arcuate Nucleus of the Rat

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          Abstract

          It is known that intracerebroventricular (ICV) administration of a low dose of interleukin-1β (IL-1β) induces hyperalgesia and that this effect can be inhibited by α-melanophore-stimulating hormone (α-MSH). To identify the part of the brain that is affected by hyperalgesia-induced IL-1β and the possible site of α-MSH inhibition, we have examined Fos expression in the rat brain in response to ICV microinjection of α-MSH and/or IL-1β. Following injection of 10 pg IL-1β, hyperalgesia was induced and Fos became expressed in the paraventricular nucleus (PVN) of the hypothalamus and in the arcuate nucleus (ARC), which contains α-MSH-producing neurons. IL-1β injection did not induce Fos expression in the pars intermedia of the pituitary gland, which contains endocrine melanotrope cells that release α-MSH into the systemic circulation. ICV co-injection of IL-1β with 30 ng α-MSH fully inhibited both hyperalgesia and Fos expression in the PVN and the ARC. We conclude that PVN neurons are activated by hyperalgesic IL-1β and propose that this effect is abolished by α-MSH possibly released from the ARC but not from the pituitary gland.

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          Most cited references 17

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          Expression of melanocortin 4 receptor mRNA in the central nervous system of the rat.

          The melanocortin 4 receptor (MC4-R) plays a pivotal role in maintaining energy homeostasis in rodents and humans. For example, MC4-R deletion or mutation results in obesity, hyperphagia, and insulin resistance. Additionally, subsets of leptin-induced autonomic responses can be blocked by melanocortin receptor antagonism, suggesting that MC4-R-expressing neurons are downstream targets of leptin. However, the critical autonomic control sites expressing MC4-Rs are still unclear. In the present study, we systematically examined the distribution of MC4-R mRNA in the adult rat central nervous system, including the spinal cord, by using in situ hybridization histochemistry (ISHH) with a novel cRNA probe. Autonomic control sites expressing MC4-R mRNA in the hypothalamus included the anteroventral periventricular, ventromedial preoptic, median preoptic, paraventricular, dorsomedial, and arcuate nuclei. The subfornical organ, dorsal hypothalamic, perifornical, and posterior hypothalamic areas were also observed to express MC4-R mRNA. Within extrahypothalamic autonomic control sites, MC4-R-specific hybridization was evident in the infralimbic and insular cortices, bed nucleus of the stria terminalis, central nucleus of the amygdala, periaqueductal gray, lateral parabrachial nucleus, nucleus of the solitary tract, dorsal motor nucleus of the vagus (DMV), and intermediolateral nucleus of the spinal cord (IML). By using dual-label ISHH, we confirmed that the cells expressing MC4-R mRNA in the IML and DMV were autonomic preganglionic neurons as cells in both sites coexpressed choline acetyltransferase mRNA. The distribution of MC4-R mRNA is consistent with the proposed roles of central melanocortin systems in feeding and autonomic regulation. Copyright 2003 Wiley-Liss, Inc.
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            Identification of a receptor for gamma melanotropin and other proopiomelanocortin peptides in the hypothalamus and limbic system.

            Corticotropin (ACTH) and melanotropin (MSH) peptides (melanocortins) are produced not only in the pituitary but also in the brain, with highest concentrations in the arcuate nucleus of the hypothalamus and the commisural nucleus of the solitary tract. We have identified a receptor for MSH and ACTH peptides that is specifically expressed in regions of the hypothalamus and limbic system. This melanocortin receptor (MC3-R) is found in neurons of the arcuate nucleus known to express proopiomelanocortin (POMC) and in a subset of the nuclei to which these neurons send projections. The MC3-R is 43% identical to the MSH receptor present in melanocytes and is strongly coupled to adenylyl cyclase. Unlike the MSH or ACTH receptors, MC3-R is potently activated by gamma-MSH peptides, POMC products that were named for their amino acid homology with alpha- and beta-MSH, but lack melanotropic activity. The primary biological role of the gamma-MSH peptides is not yet understood. The location and properties of this receptor provide a pharmacological basis for the action of POMC peptides produced in the brain and possibly a specific physiological role for gamma-MSH.
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              Localization of the melanocortin-4 receptor (MC4-R) in neuroendocrine and autonomic control circuits in the brain

               K Mountjoy (1994)
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2005
                July 2005
                29 July 2005
                : 81
                : 3
                : 167-173
                Affiliations
                aDepartment of Anatomy, Hirosaki University School of Medicine, Hirosaki, Japan; bDepartment of Anatomy, Fukushima Medical University School of Medicine, Fukushima, Japan; cDepartment of Cellular Animal Physiology, Institute for Neuroscience, Radboud University Nijmegen, Nijmegen, The Netherlands, and dDepartment of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, Nagoya, Japan
                Article
                86888 Neuroendocrinology 2005;81:167–173
                10.1159/000086888
                16015027
                © 2005 S. Karger AG, Basel

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                Page count
                Figures: 6, References: 34, Pages: 7
                Categories
                Original Paper

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