VX-induced cell death involves activation of caspase-3 in cultured rat cortical neurons

2007 ◽  
Vol 417 (2) ◽  
pp. 155-159 ◽  
Author(s):  
Catherine C. Tenn ◽  
Yushan Wang
Keyword(s):  
Cell Death ◽  
Cortical Neurons ◽  
Caspase 3 ◽  
Rat Cortical Neurons

Mechanisms of ammonia-induced cell death in rat cortical neurons: Roles of NMDA receptors and glutathione

2005 ◽  
Vol 47 (1-2) ◽  
pp. 51-57 ◽  
Author(s):  
A KLEJMAN ◽  
M WEGRZYNOWICZ ◽  
E SZATMARI ◽  
B MIODUSZEWSKA ◽  
M HETMAN ◽  
...  
Keyword(s):  
Cell Death ◽  
Nmda Receptors ◽  
Cortical Neurons ◽  
Rat Cortical Neurons

scholarly journals Caspase-8 and Caspase-3 Are Expressed by Different Populations of Cortical Neurons Undergoing Delayed Cell Death after Focal Stroke in the Rat

1999 ◽  
Vol 19 (14) ◽  
pp. 5932-5941 ◽  
Author(s):  
James J. Velier ◽  
Julie A. Ellison ◽  
Kristine K. Kikly ◽  
Patricia A. Spera ◽  
Frank C. Barone ◽  
...  
Keyword(s):  
Cell Death ◽  
Cortical Neurons ◽  
Caspase 3 ◽  
Caspase 8 ◽  
Delayed Cell Death ◽  
Different Populations

scholarly journals PAC proton-activated chloride channel contributes to acid-induced cell death in primary rat cortical neurons

Channels ◽  
2020 ◽  
Vol 14 (1) ◽  
pp. 53-58 ◽  
Author(s):  
James Osei-Owusu ◽  
Junhua Yang ◽  
Maria Del Carmen Vitery ◽  
Mengnan Tian ◽  
Zhaozhu Qiu
Keyword(s):  
Cell Death ◽  
Chloride Channel ◽  
Cortical Neurons ◽  
Rat Cortical Neurons

scholarly journals A1 adenosine receptors mediate hypoglycemia-induced neuronal injury

2004 ◽  
Vol 32 (1) ◽  
pp. 129-144 ◽  
Author(s):  
CP Turner ◽  
MR Blackburn ◽  
SA Rivkees
Keyword(s):  
Adenosine Receptors ◽  
Neuronal Death ◽  
Cortical Neurons ◽  
Caspase 3 ◽  
Neuronal Injury ◽  
Glucose Deprivation ◽  
Cellular Mechanisms ◽  
Neuronal Viability ◽  
Rat Cortical Neurons ◽  
A1 Adenosine Receptors

The cellular mechanisms that lead to neuronal death following glucose deprivation are not known, although it is recognized that hypoglycemia can lead to perturbations in intracellular calcium ([Ca2+]i) levels. Recently, activation of A1 adenosine receptors (A1AR) has been shown to alter [Ca2+]i and promote neuronal death. Thus, we examined if A1AR activation contributes to hypoglycemia-induced neuronal injury using rat cortical neurons. First, we observed that hypoglycemia was associated with large increases in neuronal adenosine release. Next, decreased neuronal viability was seen with progressive reduction in glucose concentration (25, 6, 3, 0.75 and 0 mM). Using the calcium-sensitive dye, Fluo-3, we observed both acute and long-term changes in relative [Ca2+]i during hypoglycemic conditions. Demonstrating a role for adenosine in this process, both the loss in neuronal viability and the early changes in [Ca2+]i were reversed by treatment with A1AR antagonists (8-cyclopentyl, 1,3-dipropylxanthine; 9-chloro-2-(2-furyl)(1,2,4)-triazolo(1,5-c)quinazolin-5-amine; and N-cyclopentyl-9-methyladenine). We also found that hypoglycemia induced the expression of the pro-apoptotic enzyme, caspase-3, and that A1AR antagonism reversed hypoglycemia-induced caspase-3 activity. Collectively, these data show that hypoglycemia induces A1ARs activation leading to alterations in [Ca2+]i, which plays a prominent role in leading to hypoglycemia-induced neuronal death.

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