Pflügers Archiv

, Volume 442, Issue 1, pp 49–56

The expression and regulation of depolarization-activated K+ channels in the insulin-secreting cell line INS-1

  • Jiping Su
  • Huang Yu
  • Nibedita Lenka
  • Jürgen Hescheler
  • Susanne Ullrich
Original Article

Abstract

The aim of the present study was to characterize depolarization-activated outward currents in insulin-secreting INS-1 cells and to investigate the role of K+ channels other than the KATP channels in the regulation of insulin release. Outward currents were inhibited by 4-aminopyridine (4-AP, 10 mmol/l), tetraethylammonium (TEA, 10 mmol/l) and tetrapentylammonium (TPeA, 100 µmol/l) by 55.1±3.8% (n=3), 78.1±3.2% (n=6) and 98.7±0.8% (n=5), respectively. Margatoxin (5 nmol/l) and charybdotoxin (3 µmol/l) had no effect. 4-AP inhibited mainly a fast-activating, slowly inactivating current, whereas the TEA- and TPeA-sensitive current components were slowly activating and non-inactivating. Forskolin and the forskolin analogue 1,9-dideoxyforskolin, which does not stimulate adenylyl cyclase, also inhibited the outward current, suggesting a direct effect on the channels. Using reverse transcriptase polymerase chain reaction (RT/PCR), Kv channel mRNAs of Kv1.4, Kv1.5, Kv2.1, Kv2.2, Kv3.1 and Kv3.2 were detected whereas other Kv channels, Kv1.1, Kv1.2, Kv1.3, Kv1.6 and Kv3.4 were not detected. Insulin secretion in the presence of tolbutamide (100 µmol/l) was increased by 4-AP, TEA and TPeA by 65%, 41% and 150%, respectively. Basal secretion was not affected by these blockers. Our study reveals that the opening of voltage-dependent K+ channels negatively controls insulin secretion in depolarized cells, probably by shortening the action potential thus reducing Ca2+ influx.

Action potential regulation Insulin secretion K+ channels Kv channels Patch-clamp measurements 

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Copyright information

© Springer-Verlag 2001

Authors and Affiliations

  • Jiping Su
    • 1
  • Huang Yu
    • 2
  • Nibedita Lenka
    • 1
  • Jürgen Hescheler
    • 1
  • Susanne Ullrich
    • 1
  1. 1.Institut für Neurophysiologie, Universität zu Köln, Robert-Koch-Str. 39, 50931 CologneGermany
  2. 2.Department of Physiology, The Chinese University of Hong Kong, Shatin, N.T.Hongkong

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