Molecular and Cellular Mechanism of Glutamate Receptors in Relation to Amyotrophic Lateral Sclerosis

Author(s): Yasuo Iwasaki, Ken Ikeda, Masao Kinoshita

Journal Name: Current Drug Targets - CNS & Neurological Disorders
Continued as CNS & Neurological Disorders - Drug Targets

Volume 1 , Issue 5 , 2002


Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder of the central nervous system (CNS) with an unknown etiology. This disorder is characterized clinically by muscular weakness and wasting, and pathologically by selective degeneration of the corticospinal tracts and motor neurons of the brain stem and spinal cord. Median survival following onset is 3 to 5 years. Riluzole, an antiglutamatergic agent has been shown to have modest beneficial effects on survival. Glutamate is the main excitatory neurotransmitter in the CNS and excessive activation of glutamate receptors is excitotoxic to neurons. Glutamate receptor-mediated excitotoxicity has been proposed to explain the pattern of selective neuronal cell death and clinical manifestation of ALS. Activation of glutamate receptors leading to elevation of intracellular calcium may play a major role. This review will focus on the current understanding of the molecular and cellular mechanisms of glutamate receptors in relation to ALS.

Keywords: excitatory amino acids, glutamate, glutamate receptors, excitotoxicity, amyotrophic lateral sclerosis

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Article Details

Year: 2002
Published on: 01 March, 2012
Page: [511 - 518]
Pages: 8
DOI: 10.2174/1568007023339021
Price: $65

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