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大鼠腮腺腺泡细胞内钙离子信号的数字成像

Digital imaging of intracellular Ca2+ signaling in rat parotid acinar cells.

作者信息

Tojyo Y, Tanimura A, Matsumoto Y

机构信息

Department of Dental Pharmacology, School of Dentistry, Health Sciences University of Hokkaido, Japan.

出版信息

Life Sci. 1998;62(17-18):1635-9. doi: 10.1016/s0024-3205(98)00120-9.

Abstract

Utilizing digital imaging microscopy, the receptor-mediated changes in cytosolic Ca2+ concentration ([Ca2+]i) were studied in fura-2-loaded rat parotid acinar cells. The increase in [Ca2+]i induced by carbachol was initiated in the apical pole of the acinar cells and then spread as a Ca2+ wave toward the basolateral region. A similar polarization of Ca2+ signal was observed when the acinar cells were stimulated with substance P or phenylephrine. As the microsomal Ca2+-ATPase inhibitor thapsigargin did not produce a Ca2+ wave, activation of phosphoinositide hydrolysis is probably essential to trigger the Ca2+ wave. Stimulation with 1 microM isoproterenol, a concentration which causes the maximum release of amylase, had no effect on [Ca2+]i. Extracellular ATP (0.5 mM) induced a homogeneous increase in [Ca2+]i throughout the cells in the presence of extracellular Ca2+ but did not change [Ca2+]i in the absence of extracellular Ca2+, indicating that the ATP-induced rise in [Ca2+]i, is due to Ca2+ entry.

摘要

利用数字成像显微镜,在负载fura - 2的大鼠腮腺腺泡细胞中研究了受体介导的胞质Ca2+浓度([Ca2+]i)变化。卡巴胆碱诱导的[Ca2+]i增加始于腺泡细胞的顶端,然后作为Ca2+波向基底外侧区域扩散。当用P物质或去氧肾上腺素刺激腺泡细胞时,观察到类似的Ca2+信号极化现象。由于微粒体Ca2+-ATP酶抑制剂毒胡萝卜素未产生Ca2+波,磷酸肌醇水解的激活可能是触发Ca2+波所必需的。用1 microM异丙肾上腺素刺激,该浓度可使淀粉酶最大程度释放,但对[Ca2+]i无影响。在细胞外Ca2+存在的情况下,细胞外ATP(0.5 mM)诱导整个细胞内[Ca2+]i均匀增加,但在无细胞外Ca2+时不改变[Ca2+]i,表明ATP诱导的[Ca2+]i升高是由于Ca2+内流所致。

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