title: Delayed expression of large conductance K+ channels reshaping agonist-induced currents in mouse pancreatic acinar cells.
abstract: 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.
authors.affiliation: Department of Physiology 1, Tohoku University Graduate School of Medicine, 2-1, Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan.
authors.forename: Takako
authors.initials: T
authors.lastname: Oshiro
authors.forename: Hidenori
authors.initials: H
authors.lastname: Takahashi
authors.forename: Atsushi
authors.initials: A
authors.lastname: Ohsaga
authors.forename: Satoru
authors.initials: S
authors.lastname: Ebihara
authors.forename: Hidetada
authors.initials: H
authors.lastname: Sasaki
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Maruyama
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000375:Aging / Q000502:physiology; D000818:Animals; D002712:Chlorides / Q000502:physiology; D018507:Gene Expression Regulation, Developmental / Q000502:physiology*; D066298:In Vitro Techniques; D051036:Large-Conductance Calcium-Activated Potassium Channels; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008954:Models, Biological; D046790:Pancreas, Exocrine / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D024681:Potassium Channels, Calcium-Activated / Q000502:physiology*; D021122:Protein Subunits / Q000378:metabolism
chemical_list: D002712:Chlorides; D051036:Large-Conductance Calcium-Activated Potassium Channels; D015221:Potassium Channels; D024681:Potassium Channels, Calcium-Activated; D021122:Protein Subunits; D000109:Acetylcholine