Actions of Neurotoxic β-Amyloid on Calcium Homeostasis and Viability of PC12 Cells Are Blocked by Antioxidants but Not by Calcium Channel Antagonists

2002 ◽  
Vol 67 (4) ◽  
pp. 1419-1425 ◽  
Author(s):  
Yan Zhou ◽  
Venkat Gopalakrishnan ◽  
J. Steven Richardson
1992 ◽  
Vol 118 (3) ◽  
pp. 663-670 ◽  
Author(s):  
J L Saffell ◽  
F S Walsh ◽  
P Doherty

We present evidence that direct activation of neuronal second messenger pathways in PC12 cells by opening voltage-dependent calcium channels mimics cell adhesion molecule (CAM)-induced differentiation of these cells. PC12 cells were cultured on monolayers of control 3T3 cells or 3T3 cells expressing transfected N-cadherin in the presence of KCl or a calcium channel agonist Bay K 8644. Both potassium depolarization and agonist-induced activation of calcium channels promoted substantial neurite outgrowth from PC12 cells cultured on control 3T3 monolayers and increased neurite outgrowth from those cultured on N-cadherin-expressing 3T3 monolayers. The potassium-induced response could be inhibited by L- and N-type calcium channel antagonists and by kinase inhibitor K-252b but was unaffected by pertussis toxin. In contrast activators of protein kinase C did not stimulate neurite outgrowth, and the neurite outgrowth response induced by activation of protein kinase A was not inhibited by calcium channel antagonists or pertussis toxin. These studies support the postulate that CAM-induced neuronal differentiation involves a specific transmembrane signaling pathway and suggest that activation of this pathway after CAM binding may be more important for the neurite outgrowth response than CAM-dependent adhesion per se.


Author(s):  
M. Bidya Sagar ◽  
K. Ravikumar ◽  
Y. S. Sadanandam

AbstractThe crystallographic characterization of the following three calcium channel antagonists is reported here: 2,6-dimethyl-3,5-dicarbamoyl-4-[2-nitro]-1,4-dihydropyridine (


ChemInform ◽  
1989 ◽  
Vol 20 (4) ◽  
Author(s):  
A. F. JOSLYN ◽  
E. LUCHOWSKI ◽  
D. J. TRIGGLE

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