The NMDA Receptor

Bruce G Lyeth, Larry W. Jenkins, Ronald L. Hayes

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Traumatic brain injury can produce neurochemical alterations in the brain that are of sufficient magnitude to cause neurological and cognitive deficits. These alterations are associated with a period of excessive neurotransmitter-receptor stimulation involving the N-Methyl-D-aspartate (NMDA) glutamate receptor, as well as other receptors. This abnormal stimulation can produce lasting disruption of neuronal signaling and functional deficits. A number of laboratory studies suggest that NMDA receptor antagonists administered before or soon after traumatic brain injury may provide some protection against pathophysiological effects. The likelihood that functional deficits associated with traumatic brain injury may be at least partly dependent on neurotransmitter-receptor interactions suggests that this component of the injury process may be particularly amenable to pharmacologic treatment. Although a number of highly selective and potent NMDA receptor blockers are available, issues of dosing and toxicity need to be further examined before these agents are considered for human clinical trials.

Original languageEnglish (US)
Pages (from-to)50-57
Number of pages8
JournalNeuroRehabilitation
Volume1
Issue number1
DOIs
StatePublished - 1991
Externally publishedYes

Fingerprint

N-Methyl-D-Aspartate Receptors
Neurotransmitter Receptor
Glutamate Receptors
Clinical Trials
Wounds and Injuries
Brain
Traumatic Brain Injury

ASJC Scopus subject areas

  • Physical Therapy, Sports Therapy and Rehabilitation
  • Rehabilitation
  • Clinical Neurology

Cite this

Lyeth, B. G., Jenkins, L. W., & Hayes, R. L. (1991). The NMDA Receptor. NeuroRehabilitation, 1(1), 50-57. https://doi.org/10.3233/NRE-1991-1109

The NMDA Receptor. / Lyeth, Bruce G; Jenkins, Larry W.; Hayes, Ronald L.

In: NeuroRehabilitation, Vol. 1, No. 1, 1991, p. 50-57.

Research output: Contribution to journalArticle

Lyeth, BG, Jenkins, LW & Hayes, RL 1991, 'The NMDA Receptor', NeuroRehabilitation, vol. 1, no. 1, pp. 50-57. https://doi.org/10.3233/NRE-1991-1109
Lyeth, Bruce G ; Jenkins, Larry W. ; Hayes, Ronald L. / The NMDA Receptor. In: NeuroRehabilitation. 1991 ; Vol. 1, No. 1. pp. 50-57.
@article{946663e7f6be4fa1bbcfa66670d433fa,
title = "The NMDA Receptor",
abstract = "Traumatic brain injury can produce neurochemical alterations in the brain that are of sufficient magnitude to cause neurological and cognitive deficits. These alterations are associated with a period of excessive neurotransmitter-receptor stimulation involving the N-Methyl-D-aspartate (NMDA) glutamate receptor, as well as other receptors. This abnormal stimulation can produce lasting disruption of neuronal signaling and functional deficits. A number of laboratory studies suggest that NMDA receptor antagonists administered before or soon after traumatic brain injury may provide some protection against pathophysiological effects. The likelihood that functional deficits associated with traumatic brain injury may be at least partly dependent on neurotransmitter-receptor interactions suggests that this component of the injury process may be particularly amenable to pharmacologic treatment. Although a number of highly selective and potent NMDA receptor blockers are available, issues of dosing and toxicity need to be further examined before these agents are considered for human clinical trials.",
author = "Lyeth, {Bruce G} and Jenkins, {Larry W.} and Hayes, {Ronald L.}",
year = "1991",
doi = "10.3233/NRE-1991-1109",
language = "English (US)",
volume = "1",
pages = "50--57",
journal = "NeuroRehabilitation",
issn = "1053-8135",
publisher = "IOS Press",
number = "1",

}

TY - JOUR

T1 - The NMDA Receptor

AU - Lyeth, Bruce G

AU - Jenkins, Larry W.

AU - Hayes, Ronald L.

PY - 1991

Y1 - 1991

N2 - Traumatic brain injury can produce neurochemical alterations in the brain that are of sufficient magnitude to cause neurological and cognitive deficits. These alterations are associated with a period of excessive neurotransmitter-receptor stimulation involving the N-Methyl-D-aspartate (NMDA) glutamate receptor, as well as other receptors. This abnormal stimulation can produce lasting disruption of neuronal signaling and functional deficits. A number of laboratory studies suggest that NMDA receptor antagonists administered before or soon after traumatic brain injury may provide some protection against pathophysiological effects. The likelihood that functional deficits associated with traumatic brain injury may be at least partly dependent on neurotransmitter-receptor interactions suggests that this component of the injury process may be particularly amenable to pharmacologic treatment. Although a number of highly selective and potent NMDA receptor blockers are available, issues of dosing and toxicity need to be further examined before these agents are considered for human clinical trials.

AB - Traumatic brain injury can produce neurochemical alterations in the brain that are of sufficient magnitude to cause neurological and cognitive deficits. These alterations are associated with a period of excessive neurotransmitter-receptor stimulation involving the N-Methyl-D-aspartate (NMDA) glutamate receptor, as well as other receptors. This abnormal stimulation can produce lasting disruption of neuronal signaling and functional deficits. A number of laboratory studies suggest that NMDA receptor antagonists administered before or soon after traumatic brain injury may provide some protection against pathophysiological effects. The likelihood that functional deficits associated with traumatic brain injury may be at least partly dependent on neurotransmitter-receptor interactions suggests that this component of the injury process may be particularly amenable to pharmacologic treatment. Although a number of highly selective and potent NMDA receptor blockers are available, issues of dosing and toxicity need to be further examined before these agents are considered for human clinical trials.

UR - http://www.scopus.com/inward/record.url?scp=84937105366&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84937105366&partnerID=8YFLogxK

U2 - 10.3233/NRE-1991-1109

DO - 10.3233/NRE-1991-1109

M3 - Article

AN - SCOPUS:84937105366

VL - 1

SP - 50

EP - 57

JO - NeuroRehabilitation

JF - NeuroRehabilitation

SN - 1053-8135

IS - 1

ER -