Iwatsuki N
Pflugers Arch. 1984 Dec;402(4):465-72. doi: 10.1007/BF00583949.
Membrane potential and resistance were measured in isolated segments of mouse pancreas superfused in vitro using two intracellular microelectrodes. The acinar cells were stimulated by microionophoretic ACh application from an extracellular AChCl filled micropipette. The membrane depolarization and resistance reduction evoked by short pulses of ACh stimulation were abolished by treatment with A23187 containing Ca-free solution. The subsequent exposure of the A23187-treated tissue to a Ca or Sr containing solution restored the responses to short pulses of ACh. Addition of Ba, Co, or Mn instead of Ca had no such restorative effects. Mn or Co markedly suppressed the restorative effects of Ca or Sr. It is concluded that A23187 treatment causes depletion of intracellular Ca stores. The restorative effect of Ca or Sr indicates that short pulses of ACh stimulation evoke an increase in intracellular Ca or Sr concentration. Short pulses of ACh seem to release Ca from the stimulant-sensitive Ca pool and, in addition, to increase the membrane Ca permeability.
使用两个细胞内微电极，在体外灌注的小鼠胰腺分离节段中测量膜电位和电阻。通过来自充满细胞外氯化乙酰胆碱的微吸管进行微离子电泳施加乙酰胆碱来刺激腺泡细胞。用不含钙的含A23187溶液处理后，乙酰胆碱刺激短脉冲引起的膜去极化和电阻降低被消除。随后将经A23187处理的组织暴露于含钙或锶的溶液中，恢复了对乙酰胆碱短脉冲的反应。添加钡、钴或锰代替钙没有这种恢复作用。锰或钴显著抑制钙或锶的恢复作用。得出的结论是，A23187处理导致细胞内钙库耗竭。钙或锶的恢复作用表明，乙酰胆碱刺激短脉冲引起细胞内钙或锶浓度增加。乙酰胆碱短脉冲似乎从刺激敏感钙池中释放钙，此外，还增加膜对钙的通透性。
