Methylprednisolone reduces excitatory amino acid release following experimental spinal cord injury

Danxia Liu; David J. McAdoo

doi:10.1016/0006-8993(93)90885-Q

Methylprednisolone reduces excitatory amino acid release following experimental spinal cord injury

Danxia Liu, David J. McAdoo

Neurology

Research output: Contribution to journal › Article › peer-review

64 Scopus citations

Abstract

Administration of methylprednisolone within several hours after injury to the spinal cord has been shown to reduce subsequent impairment in humans and experimental animals. Secondary damage following initial trauma is probably caused in part by the toxicity of released excitatory amino acids. We demonstrate here that methylprednisolone reduces the release of excitatory amino acids following experimental spinal cord injury in rats.

Original language	English (US)
Pages (from-to)	293-297
Number of pages	5
Journal	Brain Research
Volume	609
Issue number	1-2
DOIs	https://doi.org/10.1016/0006-8993(93)90885-Q
State	Published - Apr 23 1993

Keywords

Excitatory amino acid
Methylprednisolone
Microdialysis
Spinal cord injury

ASJC Scopus subject areas

General Neuroscience
Molecular Biology
Clinical Neurology
Developmental Biology

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10.1016/0006-8993(93)90885-Q

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title = "Methylprednisolone reduces excitatory amino acid release following experimental spinal cord injury",

abstract = "Administration of methylprednisolone within several hours after injury to the spinal cord has been shown to reduce subsequent impairment in humans and experimental animals. Secondary damage following initial trauma is probably caused in part by the toxicity of released excitatory amino acids. We demonstrate here that methylprednisolone reduces the release of excitatory amino acids following experimental spinal cord injury in rats.",

keywords = "Excitatory amino acid, Methylprednisolone, Microdialysis, Spinal cord injury",

author = "Danxia Liu and McAdoo, {David J.}",

note = "Funding Information: Acknowledgments. We thank Gregory Robak, John Nasser and Michael Hughes for technical assistance, Professors William D. Willis Jr. and Bernard Haber for helpful comments, and NIH (NSl1255 to D.J.M.), the American Paralysis Association (LB1-9104-1 to DL) and the Paralyzed Veterans of America Spinal Cord Research Foundation (#1025 to D.L.) for financial support.",

year = "1993",

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doi = "10.1016/0006-8993(93)90885-Q",

language = "English (US)",

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pages = "293--297",

journal = "Brain Research",

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T1 - Methylprednisolone reduces excitatory amino acid release following experimental spinal cord injury

AU - Liu, Danxia

AU - McAdoo, David J.

N1 - Funding Information: Acknowledgments. We thank Gregory Robak, John Nasser and Michael Hughes for technical assistance, Professors William D. Willis Jr. and Bernard Haber for helpful comments, and NIH (NSl1255 to D.J.M.), the American Paralysis Association (LB1-9104-1 to DL) and the Paralyzed Veterans of America Spinal Cord Research Foundation (#1025 to D.L.) for financial support.

PY - 1993/4/23

Y1 - 1993/4/23

N2 - Administration of methylprednisolone within several hours after injury to the spinal cord has been shown to reduce subsequent impairment in humans and experimental animals. Secondary damage following initial trauma is probably caused in part by the toxicity of released excitatory amino acids. We demonstrate here that methylprednisolone reduces the release of excitatory amino acids following experimental spinal cord injury in rats.

AB - Administration of methylprednisolone within several hours after injury to the spinal cord has been shown to reduce subsequent impairment in humans and experimental animals. Secondary damage following initial trauma is probably caused in part by the toxicity of released excitatory amino acids. We demonstrate here that methylprednisolone reduces the release of excitatory amino acids following experimental spinal cord injury in rats.

KW - Excitatory amino acid

KW - Methylprednisolone

KW - Microdialysis

KW - Spinal cord injury

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ER -

Methylprednisolone reduces excitatory amino acid release following experimental spinal cord injury

Abstract

Keywords

ASJC Scopus subject areas

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