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Main Title Astrocytes in (Patho)Physiology of the Nervous System [electronic resource] /
Author Haydon, Philip G.
Other Authors
Author Title of a Work
Parpura, Vladimir.
Publisher Springer US,
Year Published 2009
Call Number RC321-580
ISBN 9780387794921
Subjects Medicine ; Neurosciences ; Cytology ; Neurobiology
Internet Access
Description Access URL
Collation online resource.
Due to license restrictions, this resource is available to EPA employees and authorized contractors only
Contents Notes
Astrocyte Heterogeneity or Homogeneity? -- Neural Stem Cells Disguised as Astrocytes -- Neurotransmitter Receptors in Astrocytes -- Specialized Neurotransmitter Transporters in Astrocytes -- Connexin Expression (Gap Junctions and Hemichannels) in Astrocytes -- Regulation of potassium by glial cells in the centralnervous system -- Energy and Amino Acid Neurotransmitter Metabolism in Astrocytes -- Calcium ion signaling in astrocytes -- Astrocytes in Control of the Biophysical Properties of Extracellular Space -- Structural association of astrocytes with neurons and vasculature: Defining territorial boundaries -- Synaptic Information Processing by Astrocytes -- Mechanisms of transmitter release from astrocytes -- Release of Trophic Factors and Immune Molecules from Astrocytes -- Molecular approaches for studying astrocytes -- The tripartite synapse -- Glia-derived D-serine and synaptic plasticity -- Purinergic signaling in astrocyte function and interactions with neurons -- Astrocyte control of blood flow -- A Role for Glial Cells of the Neuroendocrine Brain in the Central Control of Female Sexual Development -- Physiological and Pathological Roles of Astrocyte-mediated Neuronal Synchrony -- Role of Ion Channels and Amino-Acid Transporters in the Biology of Astrocytic Tumors -- Connexins and pannexins: Two gap junction families mediating glioma growth control -- The Impact of Astrocyte Mitochondrial Metabolism on Neuroprotection During Aging -- Alexander Disease: A Genetic Disorder of Astrocytes -- Role of Astrocytes in Epilepsy -- Hepatic Encephalopathy: A Primary Astrocytopathy. Due to their lack of electrical excitability, astrocytes, a subtype of glial cell, have long been neglected as active participants in intercellular communication within the central nervous system. Astrocytes, however, possess a diverse assortment of ion channels, neurotransmitter receptors, and transport mechanisms that enable them to respond to many of the same signals that act on neurons. Astrocytes in (Patho)Physiology of the Nervous System provides readers with a comprehensive description of the physiological roles astrocytes play in regulating neuronal activity and their critical involvement in pathophysiological states of the nervous system, including gliomas, Alexander's disease, and epilepsy. This book will be particularly useful for researchers, students, and workers in the field of neurobiology and cell biology. About the authors: Vladimir Parpura, M.D., Ph.D holds both a medical degree, awarded from the University of Zagreb in Croatia in 1989, and a doctorate, received in Neuroscience and Zoology from Iowa State University in 1993. He has held faculty appointments at the Department of Zoology and Genetics, Iowa State University and the Department of Cell Biology and Neuroscience, University of California Riverside. He is presently an Associate Professor in the Department of Neurobiology, University of Alabama Birmingham. His current research focuses on understanding the modulation of calcium-dependent glutamate release from astrocytes. Philip G. Haydon, Ph.D received his doctorate from the University of Leeds, England in 1982. He has held faculty appointments at the Department of Zoology and Genetics, Iowa State University, the Department of Neuroscience at the University of Pennsylvania, and has recently moved to Tufts University School of Medicine as Professor and Chair of the Department of Neuroscience. His research focuses on the role of astrocytes in the regulation of synapses, neuronal networks and behavior as well as how these glial cells contribute to neurological disorders.