Excitotoxicity can be mediated through an interaction within the optic nerve; activation of cell body NMDA receptors is not required

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Excitotoxicity can be mediated through an interaction within the optic nerve; activation of cell body NMDA receptors is not required. / Vorwerk, C K; Naskar, R; Schuettauf, F; Zurakowski, D; McDermott, L M; Quinto, K M; Dreyer, E B.

in: VET OPHTHALMOL, Jahrgang 4, Nr. 3, 09.2001, S. 201-4.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

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@article{8cbf4d53443b4fbdb3f3679de41613d0,
title = "Excitotoxicity can be mediated through an interaction within the optic nerve; activation of cell body NMDA receptors is not required",
abstract = "Axonal trauma leads to a series of pathologic events that can culminate in neuronal death. Although the precise mechanisms of retinal ganglion cell death after optic nerve crush in the rat model have not been elucidated, glutamate antagonists can protect retinal ganglion cells after optic nerve axotomy. We therefore explored whether a glutamate congener was toxic if applied directly within the optic nerve, or if toxicity depended upon an interaction at the cell body level. NMDA reduced retinal ganglion cell survival when applied directly into the rat optic nerve. Glutamate can be toxic if administered within the optic nerve; a direct effect at the cell body is not necessary. Future work will help to additionally unravel the steps by which axotomy induces excitotoxic damage to ganglion cells, and perhaps indicate protective interventions.",
keywords = "Animals, Axotomy/veterinary, Cell Survival/drug effects, Excitatory Amino Acid Agonists/toxicity, Excitatory Amino Acid Antagonists/pharmacology, Memantine/pharmacology, N-Methylaspartate/toxicity, Nerve Crush, Optic Nerve/drug effects, Optic Nerve Injuries/pathology, Rats, Rats, Long-Evans, Receptors, N-Methyl-D-Aspartate/physiology, Retinal Ganglion Cells/drug effects",
author = "Vorwerk, {C K} and R Naskar and F Schuettauf and D Zurakowski and McDermott, {L M} and Quinto, {K M} and Dreyer, {E B}",
year = "2001",
month = sep,
doi = "10.1046/j.1463-5216.2001.00168.x",
language = "English",
volume = "4",
pages = "201--4",
journal = "VET OPHTHALMOL",
issn = "1463-5216",
publisher = "Wiley-Blackwell",
number = "3",

}

RIS

TY - JOUR

T1 - Excitotoxicity can be mediated through an interaction within the optic nerve; activation of cell body NMDA receptors is not required

AU - Vorwerk, C K

AU - Naskar, R

AU - Schuettauf, F

AU - Zurakowski, D

AU - McDermott, L M

AU - Quinto, K M

AU - Dreyer, E B

PY - 2001/9

Y1 - 2001/9

N2 - Axonal trauma leads to a series of pathologic events that can culminate in neuronal death. Although the precise mechanisms of retinal ganglion cell death after optic nerve crush in the rat model have not been elucidated, glutamate antagonists can protect retinal ganglion cells after optic nerve axotomy. We therefore explored whether a glutamate congener was toxic if applied directly within the optic nerve, or if toxicity depended upon an interaction at the cell body level. NMDA reduced retinal ganglion cell survival when applied directly into the rat optic nerve. Glutamate can be toxic if administered within the optic nerve; a direct effect at the cell body is not necessary. Future work will help to additionally unravel the steps by which axotomy induces excitotoxic damage to ganglion cells, and perhaps indicate protective interventions.

AB - Axonal trauma leads to a series of pathologic events that can culminate in neuronal death. Although the precise mechanisms of retinal ganglion cell death after optic nerve crush in the rat model have not been elucidated, glutamate antagonists can protect retinal ganglion cells after optic nerve axotomy. We therefore explored whether a glutamate congener was toxic if applied directly within the optic nerve, or if toxicity depended upon an interaction at the cell body level. NMDA reduced retinal ganglion cell survival when applied directly into the rat optic nerve. Glutamate can be toxic if administered within the optic nerve; a direct effect at the cell body is not necessary. Future work will help to additionally unravel the steps by which axotomy induces excitotoxic damage to ganglion cells, and perhaps indicate protective interventions.

KW - Animals

KW - Axotomy/veterinary

KW - Cell Survival/drug effects

KW - Excitatory Amino Acid Agonists/toxicity

KW - Excitatory Amino Acid Antagonists/pharmacology

KW - Memantine/pharmacology

KW - N-Methylaspartate/toxicity

KW - Nerve Crush

KW - Optic Nerve/drug effects

KW - Optic Nerve Injuries/pathology

KW - Rats

KW - Rats, Long-Evans

KW - Receptors, N-Methyl-D-Aspartate/physiology

KW - Retinal Ganglion Cells/drug effects

U2 - 10.1046/j.1463-5216.2001.00168.x

DO - 10.1046/j.1463-5216.2001.00168.x

M3 - SCORING: Journal article

C2 - 11722784

VL - 4

SP - 201

EP - 204

JO - VET OPHTHALMOL

JF - VET OPHTHALMOL

SN - 1463-5216

IS - 3

ER -