Chapter

Glutamate and Glutamate Receptors in Neurological Diseases

ROBERT BALÁZS, RICHARD J. BRIDGES and CARL W. COTMAN

in Excitatory Amino Acid Transmission in Health and Disease

Published in print October 2005 | ISBN: 9780195150025
Published online January 2010 | e-ISBN: 9780199865079 | DOI: http://dx.doi.org/10.1093/acprof:oso/9780195150025.003.0012
Glutamate and Glutamate Receptors in Neurological Diseases

Show Summary Details

Preview

Although glutamate (Glu) normally functions as a neurotransmitter, excess Glu can be harmful and can cause cells to degenerate. Glutamate can cause neuronal cell death by a mechanism referred to as excitotoxicity, a process of cell death of neurons and sonic glial cells resulting from excessive or prolonged activation of excitatory amino acid receptors. Excitotoxicity is a convergence point in the neurodegenerative cascade of many acute and chronic neurodegenerative disorders. In fact, a role for excitotoxicity has been implicated in the etiology of many neurodegenerative diseases, including ischemic stroke, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and epilepsy. Because Glu can cause neuronal degeneration, there are two major therapeutic approaches for neurological diseases: prevent the degeneration of neurons by controlling excitotoxicity, and modulate glutamatergic synaptic transmission and function in the surviving neurons by positive or negative regulation of glutamate receptors (GluRs). This chapter presents a snapshot of research advances regarding the ways in which glutamatergic function is involved in many neurological diseases and how this knowledge is leading to new treatment strategies.

Keywords: glutamate; glutamate receptors; neurological diseases; excitotoxicity; ischemic stroke; Alzheimer's disease; synaptic transmission; Parkinson's disease; amyotrophic lateral sclerosis; epilepsy

Chapter.  16307 words.  Illustrated.

Subjects: Neuroscience

Full text: subscription required

How to subscribe Recommend to my Librarian

Buy this work at Oxford University Press »

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.