Intracellular mechanisms of hypoxia-induced calcium increase in rat sensory neurons |
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Authors: | Lukyanetz E A Stanika R I Koval L M Kostyuk P G |
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Institution: | Bogomoletz Institute of Physiology, 01024 Kiev, Ukraine. elena@serv.biph.kiev.ua |
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Abstract: | Elevation of cytosolic level of Ca(2+) was measured by spatial screening of freshly isolated dorsal root ganglion neurons loaded with Fura-2AM after subjecting them to a moderate hypoxic solution (pO(2)=10-40 mmHg). Short exposure of neurons to hypoxia resulted in a reversible elevation of intracellular Ca(2+) to about 120% in the cell center and to 80% in the cell periphery. Such elevation could be almost completely eliminated by removal of Ca(2+) or Na(+) from external medium or application of nifedipine, an L-type calcium channel blocker. Remarkable antihypoxic efficiency (58%) was achieved by preapplication of mitochondrial protonophore CCCP. A conclusion is made that in sensory neurons the hypoxia-induced elevation of cytosolic Ca(2+) is induced by combined changes of function in three cell substructures: voltage-operated L-type Ca(2+) and Na(+) channels and Ca(2+) accumulation by mitochondria. Mitochondria are important for spatial difference in the hypoxia-induced Ca(2+) elevation due to their specific location in these neurons. |
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Keywords: | Calcium Calcium transients DRG neurons Hypoxia Mitochondria Sodium L-type calcium channels Nifedipine |
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