These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The response of pancreatic beta-cell membrane potential to potassium-induced calcium influx in the presence of glucose.
    Author: Dawson CM, Atwater I, Rojas E.
    Journal: Q J Exp Physiol; 1984 Oct; 69(4):819-30. PubMed ID: 6096913.
    Abstract:
    Membrane potential measurements were made in pancreatic beta-cells from microdissected islets from normal mice. In the presence of 11 mM glucose, depolarization of the membrane for 1 min with 50 mM potassium is followed by an inhibition of electrical activity before the normal burst pattern resumes. This inhibitory period, called the recovery time, is steady for each beta-cell after three consecutive pulses of 50 mM potassium. The mean recovery time is 109 s. During the recovery time, the membrane is hyperpolarized and the input resistance is decreased, indicating that potassium permeability is high over this period. The recovery time is dependent on the size of the depolarization: 1 min exposure to potassium concentrations below 50 mM reduces the recovery time with a half-maximal effect at 38.5 mM potassium, corresponding to -27 mV. Also, increasing the extracellular calcium concentration lengthens the recovery time. Increasing the glucose concentration, however, shortens the recovery time. It is postulated that the recovery time represents activation of the calcium-gated potassium permeability and is a reflexion of the time taken for the beta-cell to buffer the increased intracellular calcium resulting from the potassium depolarization.
    [Abstract] [Full Text] [Related] [New Search]