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lschémie cérébrale : modulations des récepteurs NMDA et mort neuronale retardée. / Benquet, Pascal; Gee, Christine E; Gerber, Urs.

In: M S-MED SCI, Vol. 24, No. 2, 01.02.2008, p. 185-90.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Benquet, P, Gee, CE & Gerber, U 2008, 'lschémie cérébrale: modulations des récepteurs NMDA et mort neuronale retardée', M S-MED SCI, vol. 24, no. 2, pp. 185-90. https://doi.org/10.1051/medsci/2008242185

APA

Benquet, P., Gee, C. E., & Gerber, U. (2008). lschémie cérébrale: modulations des récepteurs NMDA et mort neuronale retardée. M S-MED SCI, 24(2), 185-90. https://doi.org/10.1051/medsci/2008242185

Vancouver

Benquet P, Gee CE, Gerber U. lschémie cérébrale: modulations des récepteurs NMDA et mort neuronale retardée. M S-MED SCI. 2008 Feb 1;24(2):185-90. https://doi.org/10.1051/medsci/2008242185

Bibtex

@article{bb3fcf575ad4447db405f19f58d90b89,
title = "lsch{\'e}mie c{\'e}r{\'e}brale: modulations des r{\'e}cepteurs NMDA et mort neuronale retard{\'e}e",
abstract = "Transient global ischemia induces delayed neuronal death in certain cell types and brain regions while sparing cells in other areas. A key process through which oxygen-glucose deprivation triggers cell death is the excessive accumulation of the neurotransmitter glutamate leading to over excitation of neurons. In certain neurons this increase in glutamate will potentiate the NMDA type of glutamate receptor, which can then initiate cell death. This review provides an update of the neurophysiological, cellular and molecular mechanisms inducing post-ischemic plasticity of NMDA receptors, focusing on the sensitive CA1 pyramidal neurons in the hippocampus as compared to the relatively resistant neighboring CA3 neurons. Both a change in the equilibrium between protein tyrosine kinases/phosphatases and an increased density of surface NMDA receptors in response to ischemia may explain the selective vulnerability of specific cell types. Implications for the treatment of stroke and reasons for the failures of human clinical trials utilizing NMDA receptor antagonists are also discussed.",
keywords = "Cell Death, Humans, Ischemic Attack, Transient, N-Methylaspartate, Neurons, Receptors, N-Methyl-D-Aspartate",
author = "Pascal Benquet and Gee, {Christine E} and Urs Gerber",
year = "2008",
month = feb,
day = "1",
doi = "10.1051/medsci/2008242185",
language = "Franz{\"o}sisch",
volume = "24",
pages = "185--90",
journal = "M S-MED SCI",
issn = "0767-0974",
publisher = "Editions EDK",
number = "2",

}

RIS

TY - JOUR

T1 - lschémie cérébrale

T2 - modulations des récepteurs NMDA et mort neuronale retardée

AU - Benquet, Pascal

AU - Gee, Christine E

AU - Gerber, Urs

PY - 2008/2/1

Y1 - 2008/2/1

N2 - Transient global ischemia induces delayed neuronal death in certain cell types and brain regions while sparing cells in other areas. A key process through which oxygen-glucose deprivation triggers cell death is the excessive accumulation of the neurotransmitter glutamate leading to over excitation of neurons. In certain neurons this increase in glutamate will potentiate the NMDA type of glutamate receptor, which can then initiate cell death. This review provides an update of the neurophysiological, cellular and molecular mechanisms inducing post-ischemic plasticity of NMDA receptors, focusing on the sensitive CA1 pyramidal neurons in the hippocampus as compared to the relatively resistant neighboring CA3 neurons. Both a change in the equilibrium between protein tyrosine kinases/phosphatases and an increased density of surface NMDA receptors in response to ischemia may explain the selective vulnerability of specific cell types. Implications for the treatment of stroke and reasons for the failures of human clinical trials utilizing NMDA receptor antagonists are also discussed.

AB - Transient global ischemia induces delayed neuronal death in certain cell types and brain regions while sparing cells in other areas. A key process through which oxygen-glucose deprivation triggers cell death is the excessive accumulation of the neurotransmitter glutamate leading to over excitation of neurons. In certain neurons this increase in glutamate will potentiate the NMDA type of glutamate receptor, which can then initiate cell death. This review provides an update of the neurophysiological, cellular and molecular mechanisms inducing post-ischemic plasticity of NMDA receptors, focusing on the sensitive CA1 pyramidal neurons in the hippocampus as compared to the relatively resistant neighboring CA3 neurons. Both a change in the equilibrium between protein tyrosine kinases/phosphatases and an increased density of surface NMDA receptors in response to ischemia may explain the selective vulnerability of specific cell types. Implications for the treatment of stroke and reasons for the failures of human clinical trials utilizing NMDA receptor antagonists are also discussed.

KW - Cell Death

KW - Humans

KW - Ischemic Attack, Transient

KW - N-Methylaspartate

KW - Neurons

KW - Receptors, N-Methyl-D-Aspartate

U2 - 10.1051/medsci/2008242185

DO - 10.1051/medsci/2008242185

M3 - SCORING: Zeitschriftenaufsatz

C2 - 18272081

VL - 24

SP - 185

EP - 190

JO - M S-MED SCI

JF - M S-MED SCI

SN - 0767-0974

IS - 2

ER -