Store-operated Ca²⁺ entry activated by hyperpolarization in rat submandibular acinar cells

Abstract

Store-operated Ca²⁺ entry activated by hyperpolarization in rat submandibular acinar cellsYoshida, H. and Nakahari, T.Department of Physiology, Osaka Medical College, 2-7 Daigaku-cho, Takatsuki 569-8686, JapanIn rat submandibular cells, ACh evoked a biphasic increase in [Ca²⁺]_i, that is, an initial transient phase followed by a sustained phase. The initial transient phase is induced by a Ca²⁺ release from the intracellular stores and the sustained phase is maintained by a Ca²⁺ influx from the extracellular fluid, which is the so-called "store-operated Ca²⁺ entry". Store-operated Ca²⁺ entry were stimulated using 4 µM thapsigargin, sarco(end)plasmic reticulum Ca²⁺ ATPase inhibitor, in Ca²⁺-free solution followed by superfusion with control (Ca²⁺-containing) solution. This protocol resulted in a [Ca²⁺]_i increase, which was inhibited in the presence of 1 µM Gd³⁺. A restoration from 150 mM K⁺ solution(Ca²⁺-containing) to control solution also evoked an [Ca²⁺]_i increase during thapsigargin stimulation, and an [Ca²⁺]_i increase following reintroduction of Ca²⁺ during thapsigargin stimulation was completely inhibited by addition of 1 µM Gd³⁺. Although a restoration from 7.5 mM K⁺ solution to control solution did not evoke an [Ca²⁺]_i increase during thapsigargin stimulation, addition of tetraethyl ammonium into 7.5 mM K⁺ solution evoked an [Ca²⁺]_i increase. Consequently, Ca²⁺ entry pathways is activated by the store-depletion and hyperpolarization. [J Physiol Sci. 2006;56 Suppl:S150]