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Electrical characteristics of pancreatic islet cells.
Author(s) -
Matthews E K,
Sakamoto Y
Publication year - 1975
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1975.sp010897
Subject(s) - depolarization , membrane potential , intracellular , chemistry , tolbutamide , biophysics , endocrinology , electrophysiology , islet , medicine , inhibitory postsynaptic potential , population , biochemistry , biology , insulin , environmental health
1. The electrical properties of mouse pancreatic islet cells have been explored in vitro using a single intracellular micro‐electrode for both voltage recording and current injection. 2. The frequency of spontaneous electrical activity induced in islet cells by concentrations of D‐glucose greater than 2‐8 mM was enhanced by depolarizing, and reduced by hyperpolarizing, current injection. Post‐stimulus inhibition and facilitation were also observed. 3. Intracellular current injection evoked a spike potential in Krebs solution containing a low D‐glucose concentration (2–8mM), and in glucose‐free, but not Ca‐free solution. Evoked spikes were observed in approximately 10% of the cell population impaled. 4. The relationship between the rate of rise of an evoked spike and membrane potential displacement by intracellular current injection a sigmoid curve suggesting the presence of an inactivation process in spike potential genesis. 5. High [K]o, 30–50mM, induced electrical activity rarely, and then only transiently, thereafter blocking it; conditioning hyperpolarizing current tended to restore spike activity. 6. D‐600, 5 times 10‐minus 5M, blocked the electrical activity induced by D‐glucose, tolbutamide or current injection; these inhibitory effects were reversed by a threefold increase in [Ca]o to 7–68 mM. 7. From these results it is concluded that the electrical activity induced in islet cells by Dglucose, tolbutamide and current injection is due mainlu to Ca‐2+ influx and is dependent on the level of the membrane potential