Delayed expression of large conductance K+ channels reshaping agonist-induced currents in mouse pancreatic acinar cells
Epithelial secretory cells display cell-specific mechanisms of fluid secretion and express large conductance voltage- and Ca 2+ -activated K + (Maxi-K) channels that generate the membrane negativity for effective Cl â exit to the lumen. Rat and mouse pancreatic acinar cells had been thought to be...
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Veröffentlicht in: | The Journal of physiology 2005-03, Vol.563 (2), p.379-391 |
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Zusammenfassung: | Epithelial secretory cells display cell-specific mechanisms of fluid secretion and express large conductance voltage- and
Ca 2+ -activated K + (Maxi-K) channels that generate the membrane negativity for effective Cl â exit to the lumen. Rat and mouse pancreatic acinar cells had been thought to be peculiar in this sense because of the previously
reported lack of Maxi-K channels. However, this view is not entirely correct as evidenced in the present paper. Searching
for their presence in pancreatic acinar cells in mice from 5 to 84 weeks of age with patch-clamp current measurements, we
demonstrated that the expression of Maxi-K channels is regulated in an age-associated manner after birth. The expression started
at approximately 12 postnatal weeks and increased steadily up to 84 weeks. In support of this, RT-PCR could not detect mSlo
mRNA, the Maxi-K gene, at either 7 or 8 weeks but could at 58 and 64 postnatal weeks. These results suggest that a key steering
element for fluid secretion, the Maxi-K channel, is progressively re-organized in rodent pancreas. A pancreatic secretagogue,
acetylcholine, evoked Maxi-K channel current overlapping to various degrees on the previously known current response. This
suggests that the rise in internal Ca 2+ activates Maxi-K channels which reshape the mode of secretagogue-evoked current response and contribute to Cl â driving in fluid secretion in an age-associated fashion. |
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ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.2004.077834 |