The rationale for glutamate antagonists in the treatment of traumatic brain injury

J. S. Myseros, Ross Bullock

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

The recent development of potent antagonists for the most widespread neurotransmitter in the mammalian brain has opened up possibilities for many forms of therapy. The excitotoxic hypothesis implicates excessive release of excitatory amino acids (EAAs) as an important cause of brain damage, especially in acute ischemia, and chronic neurodegeneration. Focal ischemic damage and diffuse axonal injury are the major causes of brain damage after traumatic human brain injury. Evidence from animal models has shown that excitatory amino acid-induced events maybe responsible for a proportion of the posttraumatic sequelae and that these effects can be blocked by EAA antagonists. This evidence is reviewed, and the implications for human pathophysiology and treatment are discussed.

Original languageEnglish
Pages (from-to)262-271
Number of pages10
JournalAnnals of the New York Academy of Sciences
Volume765
DOIs
StatePublished - Dec 1 1995
Externally publishedYes

Fingerprint

Excitatory Amino Acid Antagonists
Brain
Excitatory Amino Acids
Diffuse Axonal Injury
Neurotransmitter Agents
Ischemia
Animal Models
Animals
Traumatic Brain Injury
Antagonist
Amino Acids
Brain Damage
Causes
Therapeutics

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

The rationale for glutamate antagonists in the treatment of traumatic brain injury. / Myseros, J. S.; Bullock, Ross.

In: Annals of the New York Academy of Sciences, Vol. 765, 01.12.1995, p. 262-271.

Research output: Contribution to journalArticle

@article{5202d9d36cf942cc9fcd8e87b765c177,
title = "The rationale for glutamate antagonists in the treatment of traumatic brain injury",
abstract = "The recent development of potent antagonists for the most widespread neurotransmitter in the mammalian brain has opened up possibilities for many forms of therapy. The excitotoxic hypothesis implicates excessive release of excitatory amino acids (EAAs) as an important cause of brain damage, especially in acute ischemia, and chronic neurodegeneration. Focal ischemic damage and diffuse axonal injury are the major causes of brain damage after traumatic human brain injury. Evidence from animal models has shown that excitatory amino acid-induced events maybe responsible for a proportion of the posttraumatic sequelae and that these effects can be blocked by EAA antagonists. This evidence is reviewed, and the implications for human pathophysiology and treatment are discussed.",
author = "Myseros, {J. S.} and Ross Bullock",
year = "1995",
month = "12",
day = "1",
doi = "10.1111/j.1749-6632.1995.tb16583.x",
language = "English",
volume = "765",
pages = "262--271",
journal = "Annals of the New York Academy of Sciences",
issn = "0077-8923",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - The rationale for glutamate antagonists in the treatment of traumatic brain injury

AU - Myseros, J. S.

AU - Bullock, Ross

PY - 1995/12/1

Y1 - 1995/12/1

N2 - The recent development of potent antagonists for the most widespread neurotransmitter in the mammalian brain has opened up possibilities for many forms of therapy. The excitotoxic hypothesis implicates excessive release of excitatory amino acids (EAAs) as an important cause of brain damage, especially in acute ischemia, and chronic neurodegeneration. Focal ischemic damage and diffuse axonal injury are the major causes of brain damage after traumatic human brain injury. Evidence from animal models has shown that excitatory amino acid-induced events maybe responsible for a proportion of the posttraumatic sequelae and that these effects can be blocked by EAA antagonists. This evidence is reviewed, and the implications for human pathophysiology and treatment are discussed.

AB - The recent development of potent antagonists for the most widespread neurotransmitter in the mammalian brain has opened up possibilities for many forms of therapy. The excitotoxic hypothesis implicates excessive release of excitatory amino acids (EAAs) as an important cause of brain damage, especially in acute ischemia, and chronic neurodegeneration. Focal ischemic damage and diffuse axonal injury are the major causes of brain damage after traumatic human brain injury. Evidence from animal models has shown that excitatory amino acid-induced events maybe responsible for a proportion of the posttraumatic sequelae and that these effects can be blocked by EAA antagonists. This evidence is reviewed, and the implications for human pathophysiology and treatment are discussed.

UR - http://www.scopus.com/inward/record.url?scp=0029549144&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029549144&partnerID=8YFLogxK

U2 - 10.1111/j.1749-6632.1995.tb16583.x

DO - 10.1111/j.1749-6632.1995.tb16583.x

M3 - Article

VL - 765

SP - 262

EP - 271

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -