NDLI: Neuroprotection by NMDA Preconditioning Against Glutamate Cytotoxicity is Mediated Through Activation of ERK 1/2, Inactivation of JNK, and by Prevention of Glutamate-Induced CREB Inactivation

Content Provider	Springer Nature Link
Author	Navon, Hila Bromberg, Yael Sperling, Oded Shani, Esther
Copyright Year	2011
Abstract	N-methyl-D-aspartate (NMDA) preconditioning is a major endogenous brain protective mechanism, activated by sub-lethal stimulation of the NMDA glutamate receptors. Selective drug activation of this mechanism is considered to be a promising neuroprotective treatment against stroke and other traumatic brain insults. We have established an experimental in vitro model of NMDA preconditioning in primary rat neuronal cultures composed of three consecutive periods: preconditioning (NMDA 50 9M for 18 h), insult (glutamic acid 200 9M for 1 h), and reperfusion (regular medium for 24 h). The insulted neuronal cultures exhibited a 2.8-fold increase in LDH release into the media during the post-insult reperfusion period, which was completely abolished in the preconditioned cultures. The alterations in the activity level of the pro-survival kinase extracellular signal-regulated kinase (ERK) 1/2, the death machine activator c-Jun N-terminal kinase (JNK), and the pro-survival transcription factor cAMP responsive element binding (CREB) were monitored in preconditioned neuronal cultures in comparison to non-preconditioned cells during the three periods of the experimental model. The preconditioned neurons exhibited increased activity levels of ERK 1/2 and decreased activity levels of JNK during all periods of the model. In addition, the non-preconditioned neurons exhibited a marked reduction in the activity level of CREB during the insult period, which was totally prevented in the preconditioned cultures. These results suggest that the neuroprotection conferred by NMDA preconditioning against glutamate cytotoxicity is mediated (at least in part) through activation of ERK 1/2, inactivation of JNK and by prevention of glutamate-induced CREB inactivation.
Starting Page	100
Ending Page	108
Page Count	9
File Format	PDF
ISSN	08958696
Journal	Journal of Molecular Neuroscience
Volume Number	46
Issue Number	1
e-ISSN	15591166
Language	English
Publisher	Humana Press Inc
Publisher Date	2011-05-10
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	CREB ERK 1/2 Glutamic acid cytotoxicity JNK Neuroprotection NMDA preconditioning Neurosciences Neurology Cell Biology Proteomics Neurochemistry
Content Type	Text
Resource Type	Article
Subject	Medicine Cellular and Molecular Neuroscience

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