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 Ca2+-activated K+ (Maxi-K) channels that generate the membrane negativity for effective Cl- 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 Ca2+ activates Maxi-K channels which reshape the mode of secretagogue-evoked current response and contribute to Cl- driving in fluid secretion in an age-associated fashion.