lschémie cérébrale
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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, Jahrgang 24, Nr. 2, 01.02.2008, S. 185-90.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -