Oxygen or glucose deprivation-induced neuronal injury in cortical cell cultures is reduced by tetanus toxin

Neuron ◽  
1992 ◽  
Vol 8 (5) ◽  
pp. 967-973 ◽  
Author(s):  
H. Monyer ◽  
R.G. Giffard ◽  
D.M. Hartley ◽  
L.L. Dugan ◽  
M.P. Goldberg ◽  
...  
Neuron ◽  
1990 ◽  
Vol 5 (2) ◽  
pp. 121-126 ◽  
Author(s):  
Hannelore Monyer ◽  
Dean M. Hartley ◽  
Dennis W. Choi

2003 ◽  
Vol 26 (4) ◽  
pp. 544-546 ◽  
Author(s):  
Hyun Joo Ha ◽  
Yong Soo Kwon ◽  
Shin Mi Park ◽  
Taekyun Shin ◽  
Jun Hong Park ◽  
...  

Metabolism ◽  
1994 ◽  
Vol 43 (9) ◽  
pp. 1108-1113 ◽  
Author(s):  
S.P. Singh ◽  
S. Ehmann ◽  
A.K. Snyder

2002 ◽  
Vol 159 (5) ◽  
pp. 821-831 ◽  
Author(s):  
Sun H. Kim ◽  
Seok J. Won ◽  
Seonghyang Sohn ◽  
Hyuk J. Kwon ◽  
Jee Y. Lee ◽  
...  

Several lines of evidence suggest that neurotrophins (NTs) potentiate or cause neuronal injury under various pathological conditions. Since NTs enhance survival and differentiation of cultured neurons in serum or defined media containing antioxidants, we set out experiments to delineate the patterns and underlying mechanisms of brain-derived neurotrophic factor (BDNF)–induced neuronal injury in mixed cortical cell cultures containing glia and neurons in serum-free media without antioxidants, where the three major routes of neuronal cell death, oxidative stress, excitotoxicity, and apoptosis, have been extensively studied. Rat cortical cell cultures, after prolonged exposure to NTs, underwent widespread neuronal necrosis. BDNF-induced neuronal necrosis was accompanied by reactive oxygen species (ROS) production and was dependent on the macromolecular synthesis. cDNA microarray analysis revealed that BDNF increased the expression of cytochrome b558, the plasma membrane-spanning subunit of NADPH oxidase. The expression and activation of NADPH oxidase were increased after exposure to BDNF. The selective inhibitors of NADPH oxidase prevented BDNF-induced ROS production and neuronal death without blocking antiapoptosis action of BDNF. The present study suggests that BDNF-induced expression and activation of NADPH oxidase cause oxidative neuronal necrosis and that the neurotrophic effects of NTs can be maximized under blockade of the pronecrotic action.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Jinsong Yang ◽  
Xiaohong Wu ◽  
Haogang Yu ◽  
Xinbiao Liao ◽  
Lisong Teng

The objective of the current research work was to evaluate the neuroprotective effect of the ethanol extract ofScutellaria baicalensis(S.B.) on the excitotoxic neuronal cell death in primary rat cortical cell cultures. The inhibitory effects of the extract were qualitatively and quantitatively estimated by phase-contrast microscopy and lactate dehydrogenase (LDH) assays. The extract exhibited a potent and dose-dependent inhibition of the glutamate-induced excitotoxicity in the culture media. Further, using radioligand binding assays, it was observed that the inhibitory effect of the extract was more potent and selective for the N-methyl-D-aspartate (NMDA) receptor-mediated toxicity. The S.B. ethanol extract competed with [3H] MDL 105,519 for the specific binding to the NMDA receptor glycine site with 50% inhibition occurring at 35.1 μg/mL. Further, NMDA receptor inactivation by the S.B. ethanol extract was concluded from the decreasing binding capability of [3H]MK-801 in the presence of the extract. Thus, S.B. extract exhibited neuroprotection against excitotoxic cell death, and this neuroprotection was mediated through the inhibition of NMDA receptor function by interacting with the glycine binding site of the NMDA receptor. Phytochemical analysis of the bioactive extract revealed the presence of six phytochemical constituents including baicalein, baicalin, wogonin, wogonoside, scutellarin, and Oroxylin A.


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