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      Role of astrocytes, microglia, and tanycytes in brain control of systemic metabolism.

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          Abstract

          Astrocytes, microglia, and tanycytes play active roles in the regulation of hypothalamic feeding circuits. These non-neuronal cells are crucial in determining the functional interactions of specific neuronal subpopulations involved in the control of metabolism. Recent advances in biology, optics, genetics, and pharmacology have resulted in the emergence of novel and highly sophisticated approaches for studying hypothalamic neuronal-glial networks. Here we summarize the progress in the field and argue that glial-neuronal interactions provide a core hub integrating food-related cues, interoceptive signals, and internal states to adapt a complex set of physiological responses operating on different timescales to finely tune behavior and metabolism according to metabolic status. This expanding knowledge helps to redefine our understanding of the physiology of food intake and energy metabolism.

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          Physiology of Astroglia.

          Alexei Verkhratsky, Maiken Nedergaard (2018)
          Astrocytes are neural cells of ectodermal, neuroepithelial origin that provide for homeostasis and defense of the central nervous system (CNS). Astrocytes are highly heterogeneous in morphological appearance; they express a multitude of receptors, channels, and membrane transporters. This complement underlies their remarkable adaptive plasticity that defines the functional maintenance of the CNS in development and aging. Astrocytes are tightly integrated into neural networks and act within the context of neural tissue; astrocytes control homeostasis of the CNS at all levels of organization from molecular to the whole organ.
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            Diversity of astrocyte functions and phenotypes in neural circuits.

            Baljit Khakh, Michael Sofroniew (2015)
            Astrocytes tile the entire CNS. They are vital for neural circuit function, but have traditionally been viewed as simple, homogenous cells that serve the same essential supportive roles everywhere. Here, we summarize breakthroughs that instead indicate that astrocytes represent a population of complex and functionally diverse cells. Physiological diversity of astrocytes is apparent between different brain circuits and microcircuits, and individual astrocytes display diverse signaling in subcellular compartments. With respect to injury and disease, astrocytes undergo diverse phenotypic changes that may be protective or causative with regard to pathology in a context-dependent manner. These new insights herald the concept that astrocytes represent a diverse population of genetically tractable cells that mediate neural circuit-specific roles in health and disease.
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              Anatomy and regulation of the central melanocortin system.

              Roger Cone (2005)
              The central melanocortin system is perhaps the best-characterized neuronal pathway involved in the regulation of energy homeostasis. This collection of circuits is unique in having the capability of sensing signals from a staggering array of hormones, nutrients and afferent neural inputs. It is likely to be involved in integrating long-term adipostatic signals from leptin and insulin, primarily received by the hypothalamus, with acute signals regulating hunger and satiety, primarily received by the brainstem. The system is also unique from a regulatory point of view in that it is composed of fibers expressing both agonists and antagonists of melanocortin receptors. Given that the central melanocortin system is an active target for development of drugs for the treatment of obesity, diabetes and cachexia, it is important to understand the system in its full complexity, including the likelihood that the system also regulates the cardiovascular and reproductive systems.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nat. Neurosci.
                Title: Nature neuroscience
                Publisher: Springer Science and Business Media LLC
                ISSN (Electronic): 1546-1726
                ISSN (Print): 1097-6256
                Publication date (Electronic): January 2019
                Volume: 22
                Issue: 1
                Affiliations
                [1 ] Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
                [2 ] Department of Physiology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
                [3 ] Inserm, Laboratory of Development and Plasticity of the Neuroendocrine Brain, Centre de Recherche Jean-Pierre Aubert, Université de Lille, Faculté de Médecine, Lille, France.
                [4 ] Univ Paris Diderot, Sorbonne Paris Cité, Paris, France.
                [5 ] Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati, OH, USA.
                [6 ] Institute of Anatomy, Leipzig University, Leipzig, Germany.
                [7 ] Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT, USA.
                [8 ] Department of Endocrinology and Metabolism, Academic Medical Center Amsterdam, Amsterdam, The Netherlands.
                [9 ] Department of Endocrinology, Hospital Infantil Universitario Niño Jesús, Instituto de Investigación la Princesa; IMDEA Food Institute, CEI UAM + CSIC; CIBEROBN, Instituto Carlos III Madrid, Madrid, Spain.
                [10 ] Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK.
                [11 ] Achucarro Center for Neuroscience, IKERBASQUE, Basque Foundation for Science, Bilbao, Spain.
                [12 ] Department of Neuroscience, University of Minnesota, Minneapolis, MN, USA.
                [13 ] Institute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Neuherberg, Germany. tschoep@helmholtz-muenchen.de.
                [14 ] Division of Metabolic Diseases, Department of Medicine, Technische Universität, Munich, Germany. tschoep@helmholtz-muenchen.de.
                Article
                Publisher Item ID: 10.1038/s41593-018-0286-y
                DOI: 10.1038/s41593-018-0286-y
                PubMed ID: 30531847
                SO-VID: b3685ea2-8e75-4c3b-92c2-5ebf6e390746
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