Excitatory amino acid-induced neuronal cell death in rat cerebellar granule cell cultures

1995 ◽  
Vol 23 (4) ◽  
pp. 599S-599S
Author(s):  
Kathleen P. PLATT ◽  
David R. BRISTOW
2007 ◽  
Vol 104 (6) ◽  
pp. 1565-1576 ◽  
Author(s):  
Yoshiaki Sato ◽  
Keiko Nakanishi ◽  
Yoshihito Tokita ◽  
Hiroko Kakizawa ◽  
Michiru Ida ◽  
...  

Amino Acids ◽  
2002 ◽  
Vol 23 (1-3) ◽  
pp. 19-25 ◽  
Author(s):  
T. Gasull ◽  
N. DeGregorio-Rocasolano ◽  
M. Enguita ◽  
J. M. Hurtan ◽  
R. Trullas

2009 ◽  
Vol 451 (1) ◽  
pp. 11-15 ◽  
Author(s):  
Takayuki Iriyama ◽  
Yoshimasa Kamei ◽  
Shiro Kozuma ◽  
Yuji Taketani

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.


2001 ◽  
Vol 21 (9) ◽  
pp. 3104-3112 ◽  
Author(s):  
Alessia Bachis ◽  
Anna M. Colangelo ◽  
Stefano Vicini ◽  
Pylord P. Doe ◽  
Maria A. De Bernardi ◽  
...  

2010 ◽  
Vol 205 (3) ◽  
pp. 263-270 ◽  
Author(s):  
Jiyeon Lee ◽  
Eunjin Lim ◽  
Yumi Kim ◽  
Endan Li ◽  
Seungjoon Park

Ghrelin is an endogenous ligand for GH secretagogue receptor type 1a (GHSR1a), and is produced and released mainly from the stomach. It has been recently demonstrated that ghrelin can function as a neuroprotective factor by inhibiting apoptotic pathways. Kainic acid (KA), an excitatory amino acid l-glutamate analog, causes neuronal death in the hippocampus; previous studies suggest that activated microglia and astrocytes actively participate in the pathogenesis of KA-induced hippocampal neurodegeneration. However, it is unclear whether ghrelin has neuroprotective effect in KA-induced hippocampal neurodegeneration. I.p. injection of KA produced typical neuronal cell death in the CA1 and CA3 pyramidal layers of the hippocampus, and the systemic administration of ghrelin significantly attenuated KA-induced neuronal cell death in these regions through the activation of GHSR1a. Ghrelin prevents KA-induced activation of microglia and astrocytes, and the expression of proinflammatory mediators tumor necrosis factor α, interleukin-1β, and cyclooxygenase-2. The inhibitory effect of ghrelin on the activation of microglia and astrocytes appears to be associated with the inhibition of matrix metalloproteinase-3 expression in damaged hippocampal neurons. Our data suggest that ghrelin has a therapeutic potential for suppressing KA-induced pathogenesis in the brain.


2002 ◽  
Vol 135 (5) ◽  
pp. 1297-1307 ◽  
Author(s):  
Ester Verdaguer ◽  
Elvira García-Jordà ◽  
Andrés Jiménez ◽  
Alessandra Stranges ◽  
Francesc X Sureda ◽  
...  

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