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Bursting Electrical Activity Generated in the Presence of KATP Channel Blockers

Pharmacology, Sensitivity to Intracellular pH and Modulation by Glucose Metabolism
  • Rosa M. Santos
  • Rui M. Barbosa
  • Célia M. Antunes
  • Amélia M. Silva
  • António P. Salgado
  • Antero J. Abrunhosa
  • Frederico C. Pereira
  • Raquel M. Seiça
  • Luís M. Rosário
Chapter
  • 117 Downloads
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 426)

Abstract

The use of the patch-clamp technique has made possible the characterization of the glucose sensitivity of a number of cation channels present in the β-cell membrane. One of these channels, the ATP-dependent K+ (KATP) channel, is specifically blocked by intracellular ATP and appears to play an essential role in the coupling of glucose metabolism to membrane depolarization and, hence, to Ca2+ influx and to the initiation of insulin release[1]. The available data indicate that the activity of the KATP channel is almost fully suppressed at 6 mM glucose, ie. a concentration which brings the membrane potential to a level just below the threshold for the appearance of electrical activity. At glucose concentrations above 7 mM the β-cell displays a pattern of bursting electrical activity which is remarkably sensitive to the hexose concentration, with the silent unexcited period (“silent phase”) being progressively reduced and the depolarized active phase (“active phase”) becoming progressively elongated as the size of the glucose stimulus increases[2]. We conclude that, while the glucose-mediated reduction in the activity of the KATP channels is indeed essential for the glucose-evoked initial depolarization of the β-cell, the modulation of bursting electrical activity by the hexose in the range 7–20 mM is apparently accounted for, at least in part, by a channel distinct from the KATP channel. The present account aims at providing evidence to support this hypothesis.

Keywords

Electrical Activity KATP Channel Mouse Islet Single Islet Active Phase Duration 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1997

Authors and Affiliations

  • Rosa M. Santos
    • 1
    • 2
  • Rui M. Barbosa
    • 1
    • 3
  • Célia M. Antunes
    • 1
  • Amélia M. Silva
    • 1
  • António P. Salgado
    • 1
  • Antero J. Abrunhosa
    • 1
  • Frederico C. Pereira
    • 1
  • Raquel M. Seiça
    • 1
    • 4
  • Luís M. Rosário
    • 1
    • 2
  1. 1.Center for Neurosciences of CoimbraUniversity of CoimbraCoimbraPortugal
  2. 2.Department of Biochemistry, Faculty of Sciences and TechnologyUniversity of CoimbraCoimbraPortugal
  3. 3.Laboratory of Instrumentation and Analysis, Faculty of PharmacyUniversity of CoimbraCoimbraPortugal
  4. 4.Institute of Physiology, Faculty of MedicineUniversity of CoimbraCoimbraPortugal

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