Role of neuronal NR2B subunit-containing NMDA receptor-mediated Ca2+ influx and astrocytic activation in cultured mouse cortical neurons and astrocytes

Synapse ◽  
2005 ◽  
Vol 59 (1) ◽  
pp. 10-17 ◽  
Author(s):  
Hideaki Kato ◽  
Minoru Narita ◽  
Mayumi Miyatake ◽  
Yoshinori Yajima ◽  
Tsutomu Suzuki
Keyword(s):  
Nmda Receptor ◽  
Cortical Neurons ◽  
Nr2b Subunit

scholarly journals Role of the fourth membrane domain of the NR2B subunit in the assembly of the NMDA receptor

Channels ◽  
2008 ◽  
Vol 2 (3) ◽  
pp. 159-160 ◽  
Author(s):  
Martin Horak ◽  
Rana A. Al-Hallaq ◽  
Kai Chang ◽  
Robert J. Wenthold
Keyword(s):  
Nmda Receptor ◽  
Nr2b Subunit ◽  
Membrane Domain

scholarly journals Ischemia-Induced Interleukin-6 as a Potential Endogenous Neuroprotective Cytokine against NMDA Receptor-Mediated Excitoxicity in the Brain

2000 ◽  
Vol 20 (6) ◽  
pp. 956-966 ◽  
Author(s):  
Carine Ali ◽  
Olivier Nicole ◽  
Fabian Docagne ◽  
Sylvain Lesne ◽  
Eric T. MacKenzie ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Nmda Receptor ◽  
Interleukin 6 ◽  
Cortical Neurons ◽  
Focal Cerebral Ischemia ◽  
Calcium Ionophore ◽  
Receptor Activation ◽  
Neuronal Cultures ◽  
The Brain

In the brain, the expression of the pleiotropic cytokine interleukin-6 (IL-6) is enhanced in various chronic or acute central nervous system disorders. However, the significance of IL-6 production in such neuropathologic states remains controversial. The present study investigated the role of IL-6 after cerebral ischemia. First, the authors showed that focal cerebral ischemia in rats early up-regulated the expression of IL-6 mRNA, without affecting the transcription of its receptors (IL-6Rα: and gp130). Similarly, the striatal injection of N-methyl-d-aspartate (NMDA) in rats, a paradigm of excitotoxic injury, activated the expression of IL-6 mRNA. The involvement of glutamatergic receptor activation was further investigated by incubating cortical neurons with NMDA or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA). NMDA and ionomycin (a calcium ionophore) up-regulated IL-6 mRNA, suggesting that neurons may produce IL-6 in response to the calcium influx mediated through NMDA receptors. The potential role of IL-6 during ischemic/excitotoxic insults was then studied by testing the effect of IL-6 against apoptotic or excitotoxic challenges in cortical cultures. IL-6 did not prevent serum deprivation- or staurosporine-induced apoptotic neuronal death, or AMPA/kainate-mediated excitotoxicity. However, in both mixed and pure neuronal cultures, IL-6 dose-dependently protected neurons against NMDA toxicity. This effect was blocked by a competitive inhibitor of IL-6. Overall, the results suggest that the up-regulation of IL-6 induced by cerebral ischemia could represent an endogenous neuroprotective mechanism against NMDA receptor-mediated injury.

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