Mogami H, Nakano K, Tepikin A V, Petersen O H
Medical Research Council Secretory Control Research Group, Physiological Laboratory, University of Liverpool, United Kingdom.
Cell. 1997 Jan 10;88(1):49-55. doi: 10.1016/s0092-8674(00)81857-7.
Intracellular Ca2+ store depletion induces Ca2+ entry across the plasma membrane, allowing the store to recharge. In our experiments, Ca2+ stores in pancreatic acinar cells were depleted by acetylcholine (ACh) stimulation in Ca2+-free solution. Thereafter, Ca2+ entry was only allowed through a CaCl2-containing pipette attached to the basal membrane. Recharging intracellular Ca2+ stores via a patch pipette occurred without a rise in the cytosolic Ca2+ concentration and depended on the operation of a thapsigargin-sensitive Ca2+ pump. After a period of focal Ca2+ entry, ACh could again evoke a rise in the cytosolic Ca2+ concentration, and this rise always started in the apical secretory pole. Recharging the apical Ca2+ store therefore depends on Ca2+ flow through a tunnel from the basal to the secretory pole, and the endoplasmic reticulum Ca2+ pump is essential for this process.
细胞内钙库耗竭会诱导钙离子通过质膜进入,使钙库得以重新充盈。在我们的实验中,在无钙溶液中通过乙酰胆碱(ACh)刺激耗尽胰腺腺泡细胞中的钙库。此后,仅允许钙离子通过连接在基底膜上的含氯化钙的移液管进入。通过膜片移液管对细胞内钙库进行重新充盈时,胞质钙离子浓度并未升高,且依赖于毒胡萝卜素敏感的钙泵的运作。在局部钙离子进入一段时间后,ACh可再次引发胞质钙离子浓度升高,且这种升高总是始于顶端分泌极。因此,顶端钙库的重新充盈依赖于钙离子从基底流向分泌极并通过一个通道,而内质网钙泵对这一过程至关重要。