Astrocytes in (Patho)Physiology of the Nervous System - Hardcover

Hardcover

ISBN 10: 0387794913 ISBN 13: 9780387794914

Publisher: Springer, 2008

Synopsis

Astrocytes were the original neuroglia that Ramón y Cajal visualized in 1913 using a gold sublimate stain. This stain targeted intermediate filaments that we now know consist mainly of glial fibrillary acidic protein, a protein used today as an astrocytic marker. Cajal described the morphological diversity of these cells with some ast- cytes surrounding neurons, while the others are intimately associated with vasculature. We start the book by discussing the heterogeneity of astrocytes using contemporary tools and by calling into question the assumption by classical neuroscience that neurons and glia are derived from distinct pools of progenitor cells. Astrocytes have long been neglected as active participants in intercellular communication and information processing in the central nervous system, in part due to their lack of electrical excitability. The follow up chapters review the “nuts and bolts” of ast- cytic physiology; astrocytes possess a diverse assortment of ion channels, neu- transmitter receptors, and transport mechanisms that enable the astrocytes to respond to many of the same signals that act on neurons. Since astrocytes can detect chemical transmitters that are released from neurons and can release their own extracellular signals there is an increasing awareness that they play physiological roles in regulating neuronal activity and synaptic transmission. In addition to these physiological roles, it is becoming increasingly recognized that astrocytes play critical roles during pathophysiological states of the nervous system; these states include gliomas, Alexander disease, and epilepsy to mention a few.

About this title

From the Back Cover

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 andbehavior as well as how these glial cells contribute to neurological disorders.

Edition details

• Publisher: Springer
• Publication date: 2008
• Language: English
• ISBN 10: 0387794913
• ISBN 13: 9780387794914
• Binding: Hardcover
• Number of pages: 758
• Editor: Parpura Vladimir, Haydon Philip G.