Milla 2011 Cell Calcium: Difference between revisions

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Milla J, Montesinos MS, Machado JD, Borges R, Alonso E, Moreno-Ortega AJ, Cano-Abad MF, García AG, Ruiz-Nuño A (2011) Ouabain enhances exocytosis through the regulation of calcium handling by the endoplasmic reticulum of chromaffin cells. Cell Calcium 50:332-42.

» PMID: 21741086

Milla J, Montesinos MS, Machado JD, Borges R, Alonso E, Moreno-Ortega AJ, Cano-Abad MF, Garcia AG, Ruiz-Nuno A (2011) Cell Calcium

Abstract: The augmentation of neurotransmitter and hormone release produced by ouabain inhibition of plasmalemmal Na⁺/K⁺-ATPase (NKA) is well established. However, the mechanism underlying this action is still controversial. Here we have shown that in bovine adrenal chromaffin cells ouabain diminished the mobility of chromaffin vesicles, an indication of greater number of docked vesicles at subplasmalemmal exocytotic sites. On the other hand, ouabain augmented the number of vesicles undergoing exocytosis in response to a K⁺ pulse, rather than the quantal size of single vesicles. Furthermore, ouabain produced a tiny and slow Ca²⁺ release from the endoplasmic reticulum (ER) and gradually augmented the transient elevations of the cytosolic Ca²⁺ concentrations ([Ca²⁺]c) triggered by K⁺ pulses. These effects were paralleled by gradual increments of the transient catecholamine release responses triggered by sequential K+ pulses applied to chromaffin cell populations treated with ouabain. Both, the increases of Ka⁺-elicited [Ca²⁺]c and secretion in ouabain-treated cells were blocked by thapsigargin (THAPSI), 2-aminoethoxydiphenyl borate (2-APB) and caffeine. These results are compatible with the view that ouabain may enhance the ER Ca²⁺ load and facilitate the Ca²⁺-induced-Ca²⁺ release (CICR) component of the [Ca²⁺]c signal generated during K⁺ depolarisation. This could explain the potentiating effects of ouabain on exocytosis.

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 {{Publication
 |title=Milla J, Montesinos MS, Machado JD, Borges R, Alonso E, Moreno-Ortega AJ, Cano-Abad MF, García AG, Ruiz-Nuño A (2011) Ouabain enhances exocytosis through the regulation of calcium handling by the endoplasmic reticulum of chromaffin cells. Cell Calcium 50:332-42.
 |info=[https://www.ncbi.nlm.nih.gov/pubmed/21741086 PMID: 21741086]
 |authors=Milla J, Montesinos MS, Machado JD, Borges R, Alonso E, Moreno-Ortega AJ, Cano-Abad MF, Garcia AG, Ruiz-Nuno A
 |year=2011
 |journal=Cell Calcium
-|abstract=The augmentation of neurotransmitter and hormone release produced by ouabain inhibition of plasmalemmal Na<sup>+</sup>/K<sup>+</sup>-ATPase (NKA) is well established. However, the mechanism underlying this action is still controversial. Here we have shown that in bovine adrenal chromaffin cells ouabain diminished the mobility of chromaffin vesicles, an indication of greater number of docked vesicles at subplasmalemmal exocytotic sites. On the other hand, ouabain augmented the number of vesicles undergoing exocytosis in response to a K<sup>+</sup> pulse, rather than the quantal size of single vesicles. Furthermore, ouabain produced a tiny and slow Ca<sup>2+</sup> release from the endoplasmic reticulum (ER) and gradually augmented the transient elevations of the cytosolic Ca<sup>2+</sup> concentrations ([Ca<sup>2+</sup>]c) triggered by K<sup>+</sup> pulses. These effects were paralleled by gradual increments of the transient catecholamine release responses triggered by sequential K+ pulses applied to chromaffin cell populations treated with ouabain. Both, the increases of Ka<sup>+</sup>-elicited [Ca<sup>2+</sup>]c and secretion in ouabain-treated cells were blocked by thapsigargin (THAPSI), 2-aminoethoxydiphenyl borate (2-APB) and caffeine. These results are compatible with the view that ouabain may enhance the ER Ca<sup>2+</sup> load and facilitate the Ca<sup>2+</sup>-induced-Ca<sup>2+</sup> release (CICR) component of the [Ca<sup>2+</sup>]c signal generated during K+ depolarisation. This could explain the potentiating effects of ouabain on exocytosis.
+|abstract=The augmentation of neurotransmitter and hormone release produced by ouabain inhibition of plasmalemmal Na<sup>+</sup>/K<sup>+</sup>-ATPase (NKA) is well established. However, the mechanism underlying this action is still controversial. Here we have shown that in bovine adrenal chromaffin cells ouabain diminished the mobility of chromaffin vesicles, an indication of greater number of docked vesicles at subplasmalemmal exocytotic sites. On the other hand, ouabain augmented the number of vesicles undergoing exocytosis in response to a K<sup>+</sup> pulse, rather than the quantal size of single vesicles. Furthermore, ouabain produced a tiny and slow Ca<sup>2+</sup> release from the endoplasmic reticulum (ER) and gradually augmented the transient elevations of the cytosolic Ca<sup>2+</sup> concentrations ([Ca<sup>2+</sup>]c) triggered by K<sup>+</sup> pulses. These effects were paralleled by gradual increments of the transient catecholamine release responses triggered by sequential K+ pulses applied to chromaffin cell populations treated with ouabain. Both, the increases of Ka<sup>+</sup>-elicited [Ca<sup>2+</sup>]c and secretion in ouabain-treated cells were blocked by thapsigargin (THAPSI), 2-aminoethoxydiphenyl borate (2-APB) and caffeine. These results are compatible with the view that ouabain may enhance the ER Ca<sup>2+</sup> load and facilitate the Ca<sup>2+</sup>-induced-Ca<sup>2+</sup> release (CICR) component of the [Ca<sup>2+</sup>]c signal generated during K<sup>+</sup> depolarisation. This could explain the potentiating effects of ouabain on exocytosis.
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