Benquet, Pascal; Gee, Christine E; Gerber, Urs (2008). Transient brain ischemia: NMDA receptor modulation and delayed neuronal death. Médecine Sciences, 24(2):185-190.
View at publisher
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.
238 downloads since deposited on 06 Jan 2010
44 downloads since 12 months
|Item Type:||Journal Article, refereed, further contribution|
|Communities & Collections:||04 Faculty of Medicine > Brain Research Institute|
|Dewey Decimal Classification:||570 Life sciences; biology
610 Medicine & health
|Deposited On:||06 Jan 2010 14:35|
|Last Modified:||01 Dec 2013 17:23|
|Free access at:||Official URL. An embargo period may apply.|
Users (please log in): suggest update or correction for this item
Repository Staff Only: item control page