Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/9448
Title: Bis(7)-tacrine prevents glutamate-induced excitotoxicity more potently than memantine by selectively inhibiting NMDA receptors
Authors: Liu, YW
Li, CY
Luo, JL
Li, WM
Fu, HJ
Lao, YZ
Liu, LJ
Pang, YP
Chang, DC
Li, ZW
Peoples, RW
Ai, YX
Han, YF 
Keywords: Acetylcholinesterase inhibitor
Bis(7)-tacrine
Excitotoxicity
Glutamate receptor
Memantine
NMDA receptor
Issue Date: 2008
Publisher: Academic Press
Source: Biochemical and biophysical research communications, 2008, v. 369, no. 4, p. 1007-1011 How to cite?
Journal: Biochemical and biophysical research communications 
Abstract: We have recently reported that bis(7)-tacrine could prevent glutamate-induced neuronal apoptosis through NMDA receptors. In this study, we demonstrated that in cultured rat cortical neurons, bis(7)-tacrine (IC 50, 0.02 μM) prevented glutamate-induced excitotoxicity more substantially than memantine (IC 50, 0.7 μM). In addition, bis(7)-tacrine was more efficient than memantine in buffering the intracellular Ca 2+ triggered by glutamate. In cultured rat hippocampal neurons, bis(7)-tacrine inhibited 50 μM NMDA-activated current in a concentration-dependent manner with an IC 50 of 0.68 ± 0.07 μM, which is five times more potent than that produced by memantine (IC 50, 3.41 ± 0.36 μM; p < 0.05). By contrast, bis(7)-tacrine, up to 5 μM, did not significantly affect the current activated by 50 μM AMPA or 50 μM kainate. These results suggest that bis(7)-tacrine is more potent than memantine against glutamate-induced neurotoxicity by selectively inhibiting NMDA-activated current.
URI: http://hdl.handle.net/10397/9448
ISSN: 0006-291X
EISSN: 1090-2104
DOI: 10.1016/j.bbrc.2008.02.133
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