The effect of inactivation of calcium channels by intracellular Ca2+ ions in the bursting pancreatic beta-cells.
The effect of inactivation of calcium channels by intracellular Ca2+ ions in the bursting pancreatic beta-cells.
复制标题
破裂的胰腺 β 细胞中细胞内 Ca2 离子对钙通道失活的影响。
DOI:
10.1007/bf02797114
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发表时间:
1987
期刊:
影响因子:
--
通讯作者:
Chay,TR
中科院分区:
文献类型:
--
作者:
Chay,TR
Based on recently determined ionic channel properties, a simple theoretical model for the burst activity of the pancreatic β-cell is formulated in this paper. The model contains an inward voltage-activated Ca2+current which is inactivated by intracellular calcium ions and an outward K+current that is activated by the membrane potential. The probability of opening of the channel gates is represented by Boltzmann equations. Our model is applicable in a regime where an ATP-blockable K+channel is inhibited. In this regime, glucose is treated as an activator for the rate of efflux of intracellular Ca2+ions, and hence its effect is equated tokCa, the efflux rate constant. In addition, intracellular H+ion, which is a byproduct of the glycolytic metabolic process, is treated as a competitive inhibitor for Ca2+ion. Since H+is a competitive inhibitor (according to our assumption), its effect is equated to the strength of the Caidissociation constantKh. In the model, a Ca2+binding site is assumed to exist in the inner membrane of the voltage-gated Ca2+channel. The model predicts that a spike and burst electrical pattern can be generated by varyingkcaand that a given pattern may produce different levels of intracellular Ca2+depending onKh. In other words, it predicts that levels of [Ca2+]ican be separated from the electrical activity by controlling the concentration of glucose and pH appropriately. This may account for the experimental observation of Lebrun et al. (1985) that insulin secretion is not correlated to the burst of electrical activity.