Keizer J, Smolen P
Institute of Theoretical Dynamics, University of California, Davis 95616.
Proc Natl Acad Sci U S A. 1991 May 1;88(9):3897-901. doi: 10.1073/pnas.88.9.3897.
We investigate the hypothesis that two classes of Ca2+ currents, one quickly inactivated by Ca2+ and one slowly inactivated by voltage, contribute to bursting electrical activity in pancreatic islets. A mathematical model of these currents is fit to the experimental whole-cell current-voltage and inactivation profiles, thereby fixing the Ca2+ conductance and all activation and inactivation parameters. Incorporating these currents into a model that includes delayed rectifier K+ channels and ATP-sensitive K+ channels, we show that only abnormal bursting is obtained. Modification of activation parameters to increase Ca2+ channel open times, as suggested by experiment, yields a more robust bursting similar to that observed in intact islets. This reinforces the suggestion that in addition to ATP-sensitive K+ channels, Ca2+ channels may serve as glucose sensors in the beta cell.
两类钙电流，一类被钙离子快速失活，另一类被电压缓慢失活，共同促成胰岛中的爆发式电活动。这些电流的数学模型与实验全细胞电流 - 电压及失活曲线相拟合，从而确定了钙电导以及所有激活和失活参数。将这些电流纳入一个包含延迟整流钾通道和ATP敏感性钾通道的模型中，我们发现只能得到异常的爆发式活动。按照实验建议修改激活参数以增加钙通道开放时间，会产生一种更稳健的爆发式活动，类似于在完整胰岛中观察到的情况。这进一步支持了这样的观点，即除了ATP敏感性钾通道外，钙通道可能在β细胞中充当葡萄糖传感器。
