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George H. Bresnick, MD

Arch Ophthalmol. 1989;107(3):339-341.

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

A series of recent articles in the neurology literature described an interesting new putative mechanism for central nervous system damage caused by ischemia, hypoglycemia, and, possibly, some hereditary neurologic degenerations as well (the latter include Huntington's disease and a type of olivopontocerebellar atrophy).^1,2 The common mechanism thought to underlie these diverse pathologic processes is the presence of excessive amino acid neurotransmitters, specifically, glutamate and aspartate, which can lead to neuronal cell swelling, lysis, and death. The term excitotoxin has been used to describe the dual action of these amino acid substances: neuronal excitation under normal conditions and cell toxicity when they are present in excess.3

See also p 409.

It has been known for some time that glutamate, when administered systemically or applied locally to the brain or retina in animal experiments, causes a degeneration of neuronal tissue. In the neonatal mouse and rat, for example, systemic administration . . . [Full Text PDF of this Article]

Author Affiliations
Madison, Wis

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