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NMDA receptors and the differential ischemic vulnerability of hippocampal neurons

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NMDA receptors and the differential ischemic vulnerability of hippocampal neurons. / Gee, Christine E; Benquet, Pascal; Raineteau, Olivier; Rietschin, Lotty; Kirbach, Sebastian W; Gerber, Urs.

In: EUR J NEUROSCI, Vol. 23, No. 10, 01.05.2006, p. 2595-603.

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

Harvard

Gee, CE, Benquet, P, Raineteau, O, Rietschin, L, Kirbach, SW & Gerber, U 2006, 'NMDA receptors and the differential ischemic vulnerability of hippocampal neurons', EUR J NEUROSCI, vol. 23, no. 10, pp. 2595-603. https://doi.org/10.1111/j.1460-9568.2006.04786.x

APA

Gee, C. E., Benquet, P., Raineteau, O., Rietschin, L., Kirbach, S. W., & Gerber, U. (2006). NMDA receptors and the differential ischemic vulnerability of hippocampal neurons. EUR J NEUROSCI, 23(10), 2595-603. https://doi.org/10.1111/j.1460-9568.2006.04786.x

Vancouver

Gee CE, Benquet P, Raineteau O, Rietschin L, Kirbach SW, Gerber U. NMDA receptors and the differential ischemic vulnerability of hippocampal neurons. EUR J NEUROSCI. 2006 May 1;23(10):2595-603. https://doi.org/10.1111/j.1460-9568.2006.04786.x

Bibtex

@article{297a66eec92647e7909a135808ce38b6,
title = "NMDA receptors and the differential ischemic vulnerability of hippocampal neurons",
abstract = "Transient cerebral ischemia causes an inhomogeneous pattern of cell death in the brain. We investigated mechanisms, which may underlie the greater susceptibility of hippocampal CA1 vs. CA3 pyramidal cells to ischemic insult. Using an in vitro oxygen-glucose deprivation (OGD) model of ischemia, we found that N-methyl-D-aspartate (NMDA) responses were enhanced in the more susceptible CA1 pyramidal cells and transiently depressed in the resistant CA3 pyramidal cells. The long-lasting potentiation of NMDA responses in CA1 cells was associated with delayed cell death and was prevented by blocking tyrosine kinase-dependent up-regulation of NMDA receptor function. In CA3 cells, the energy deprivation-induced transient depression of NMDA responses was converted to potentiation by blocking protein phosphatase signalling. These results suggest that energy deprivation differentially shifts the intracellular equilibrium between the tyrosine kinase and phosphatase activities that modulate NMDA responses in CA1 and CA3 pyramidal cells. Therapeutic modulation of tyrosine phosphorylation may thus prove beneficial in mitigating ischemia-induced neuronal death in vulnerable brain areas.",
keywords = "Animals, Cell Death, Enzyme Activation, Enzyme Inhibitors, Excitatory Amino Acid Antagonists, Hippocampus, Hypoxia-Ischemia, Brain, Immunohistochemistry, Long-Term Potentiation, Organ Culture Techniques, Patch-Clamp Techniques, Phosphoric Monoester Hydrolases, Protein-Tyrosine Kinases, Pyramidal Cells, Rats, Rats, Wistar, Receptors, N-Methyl-D-Aspartate",
author = "Gee, {Christine E} and Pascal Benquet and Olivier Raineteau and Lotty Rietschin and Kirbach, {Sebastian W} and Urs Gerber",
year = "2006",
month = may,
day = "1",
doi = "10.1111/j.1460-9568.2006.04786.x",
language = "English",
volume = "23",
pages = "2595--603",
journal = "EUR J NEUROSCI",
issn = "0953-816X",
publisher = "Wiley-Blackwell",
number = "10",

}

RIS

TY - JOUR

T1 - NMDA receptors and the differential ischemic vulnerability of hippocampal neurons

AU - Gee, Christine E

AU - Benquet, Pascal

AU - Raineteau, Olivier

AU - Rietschin, Lotty

AU - Kirbach, Sebastian W

AU - Gerber, Urs

PY - 2006/5/1

Y1 - 2006/5/1

N2 - Transient cerebral ischemia causes an inhomogeneous pattern of cell death in the brain. We investigated mechanisms, which may underlie the greater susceptibility of hippocampal CA1 vs. CA3 pyramidal cells to ischemic insult. Using an in vitro oxygen-glucose deprivation (OGD) model of ischemia, we found that N-methyl-D-aspartate (NMDA) responses were enhanced in the more susceptible CA1 pyramidal cells and transiently depressed in the resistant CA3 pyramidal cells. The long-lasting potentiation of NMDA responses in CA1 cells was associated with delayed cell death and was prevented by blocking tyrosine kinase-dependent up-regulation of NMDA receptor function. In CA3 cells, the energy deprivation-induced transient depression of NMDA responses was converted to potentiation by blocking protein phosphatase signalling. These results suggest that energy deprivation differentially shifts the intracellular equilibrium between the tyrosine kinase and phosphatase activities that modulate NMDA responses in CA1 and CA3 pyramidal cells. Therapeutic modulation of tyrosine phosphorylation may thus prove beneficial in mitigating ischemia-induced neuronal death in vulnerable brain areas.

AB - Transient cerebral ischemia causes an inhomogeneous pattern of cell death in the brain. We investigated mechanisms, which may underlie the greater susceptibility of hippocampal CA1 vs. CA3 pyramidal cells to ischemic insult. Using an in vitro oxygen-glucose deprivation (OGD) model of ischemia, we found that N-methyl-D-aspartate (NMDA) responses were enhanced in the more susceptible CA1 pyramidal cells and transiently depressed in the resistant CA3 pyramidal cells. The long-lasting potentiation of NMDA responses in CA1 cells was associated with delayed cell death and was prevented by blocking tyrosine kinase-dependent up-regulation of NMDA receptor function. In CA3 cells, the energy deprivation-induced transient depression of NMDA responses was converted to potentiation by blocking protein phosphatase signalling. These results suggest that energy deprivation differentially shifts the intracellular equilibrium between the tyrosine kinase and phosphatase activities that modulate NMDA responses in CA1 and CA3 pyramidal cells. Therapeutic modulation of tyrosine phosphorylation may thus prove beneficial in mitigating ischemia-induced neuronal death in vulnerable brain areas.

KW - Animals

KW - Cell Death

KW - Enzyme Activation

KW - Enzyme Inhibitors

KW - Excitatory Amino Acid Antagonists

KW - Hippocampus

KW - Hypoxia-Ischemia, Brain

KW - Immunohistochemistry

KW - Long-Term Potentiation

KW - Organ Culture Techniques

KW - Patch-Clamp Techniques

KW - Phosphoric Monoester Hydrolases

KW - Protein-Tyrosine Kinases

KW - Pyramidal Cells

KW - Rats

KW - Rats, Wistar

KW - Receptors, N-Methyl-D-Aspartate

U2 - 10.1111/j.1460-9568.2006.04786.x

DO - 10.1111/j.1460-9568.2006.04786.x

M3 - SCORING: Journal article

C2 - 16817862

VL - 23

SP - 2595

EP - 2603

JO - EUR J NEUROSCI

JF - EUR J NEUROSCI

SN - 0953-816X

IS - 10

ER -