| 17045260 |
Orozco C, Garcia-de-Diego AM, Arias E, Hernandez-Guijo JM, Garcia AG, Villarroya M, Lopez MG: Depolarization preconditioning produces cytoprotection against veratridine-induced chromaffin cell death. Eur J Pharmacol. 2006 Dec 28;553(1-3):28-38. Epub 2006 Sep 12.
The hypothesis that K (+) channels and cell depolarization are involved in neuronal death and neuroprotection was tested in bovine chromaffin cells subjected to two treatment periods: the first period (preconditioning period) lasted 6 to 48 h and consisted of treatment with high K (+) solutions or with tetraethylammonium (TEA), a K (+) channel blocker; the second period consisted of incubation with veratridine for 24 h, to cause cell damage. Preconditioning with high K (+) (20-80 mM) or TEA (10-30 mM) for 24 h caused 20-60% cytoprotection against veratridine-induced cell death in bovine chromaffin cells. The absence of Ca (2+) ions during the first 9 h of an 18-h preconditioning period abolished the cytoprotection. Preconditioning with K (+) or TEA increased by 2.5-fold the expression of brain-derived neurotrophic factor and by nearly 2-fold the expression of the antiapoptotic protein Bcl-2. However, preconditioning did not modify the veratridine-evoked Ca (2+) signal. High K (+) shifted the Em by about 10 mV and TEA evoked a transient burst of action potentials superimposed on a sustained depolarization. We conclude that preconditioning may protect chromaffin cells from death by blocking K (+) channels that depolarize the cell and cause a cytosolic Ca (2+) signal, leading to enhanced expression of BDNF and Bcl-2. |
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