Abstract
Large conductance, voltage- and Ca2+-activated K+ channel (Maxi-K) is distributed in a variety of epithelial secretory cells, seemingly displaying cell-specific mechanisms of fluid secretion, where an effective Cl− exit takes place through the membrane negativity created by the activation of K+ channels. Rat and mouse pancreatic acinar cells are peculiar in this sense because of the lack of Maxi-K channel, which, once activated, can fairly influence the membrane potential due to its large unitary conductance. However, as evidenced here, this is not entirely correct. The expression of Maxi-K channels is controlled in an age-dependent manner. We studied their presence in mouse pancreatic acinar cells, during the animal age from 5- to 84-week after birth, with patch-clamp measurements and RT-PCR detection of mRNA of mSlo, the mouse Maxi-K channel gene. Channel activity on the plasma membrane started to appear around 12 postnatal weeks and the rate of the channel presence steeply increased up to 84 weeks. We could detect mSlo mRNA in pancreas of old (58 and 64 weeks) animals but not of young (7 or 8 weeks). Acetylcholine activated Maxi-K channels most immediately after its administration among the pancreatic Ca2+-activated ion channels, implying Maxi-K channels locate very close to the zone triggering the first rise in internal Ca2+. These results suggest that the pancreatic secretory machinery is progressively reorganized and the mode of fluid secretion is reshaped with aging. [Jpn J Physiol 54 Suppl:S132 (2004)]
