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Nicholas J. Maragakis, MD; Jeffrey D. Rothstein, MD, PhD

Arch Neurol. 2001;58:365-370.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

Glutamate is the primary excitatory amino acid neurotransmitter in the human brain. It is important in synaptic plasticity, learning, and development. Its activity at the synaptic cleft is carefully balanced by receptor inactivation and glutamate reuptake. When this balance is upset, excess glutamate can itself become neurotoxic.

The neurotoxic properties of glutamate were first demonstrated in 1957 by Lucas and Newhouse,¹ who showed that systemic administration of glutamate to infant mice caused retinal degeneration. Over the last 4 decades, a direct correlation between the neuroexcitatory and neurotoxic properties of glutamate has been linked to activation of excitatory amino acid receptors.^{2, 3, 4, 5} This overactivation leads to an enzymatic cascade of events ultimately resulting in cell death.

Regulation of synaptic transmission and glutamate levels in the synaptic cleft is performed by glutamate transporters. Glutamate transport is a sodium- and potassium-coupled process that is capable . . . [Full Text of this Article]

HUMAN GLUTAMATE TRANSPORTERS

NEUROSCIENTIFIC STUDY OF GLUTAMATE TRANSPORTER DYSFUNCTION

GLUTAMATE TRANSPORT AND HUMAN DISEASE

Amyotrophic Lateral Sclerosis

Alzheimer Disease

Stroke/Ischemia

Epilepsy

APPLICATIONS FOR DIAGNOSIS

COMMENT

From the Department of Neurology, Johns Hopkins University, Baltimore, Md.

Corresponding author and reprints: Jeffrey D. Rothstein, Department of Neurology, Johns Hopkins University, Meyer 6-109, 600 N Wolfe St, Baltimore, MD 21287 (e-mail: jrothste@jhmi.edu).

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