Inhibition of L-type calcium channels by internal GTP [γS] in mouse pancreatic β cells

Carina Ämmälä, Per Olof Berggren, Krister Bokvist, Patrik Rorsman

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Pretreatment of pancreatic β cells with pertussis toxin resulted in a 30% increase in peak whole-cell Ca2+ currents recorded in the absence of exogenous intracellular guanine nucleotides. Intracellular application of 90 μM GTP[γS], by liberation from a caged precursor, resulted in 40% reduction of the peak Ca2+ current irrespective of whether the current was carried by Ca2+ or Ba2+. Effects on the delayed outward K+ current were small and restricted to a transient Ca2+-dependent K+ current component. Inhibition by GTP[γS] of the Ca2+ current was not mimicked by standard GTP and could not be prevented either by pretreatment with pertussis toxin or by inclusion of GDP[βS] or cyclic AMP in the intracellular medium. The inhibitory effect of GTP[γS] could be counteracted by a prepulse to a large depolarizing voltage. A similar effect of a depolarizing prepulse was observed in control cells with no exogenous guanine nucleotides. These observations indicate that inhibition of β cell Ca2+ current by G protein activation results from direct interaction with the channel and does not involve second-messenger systems. Our findings also suggest that the β cell Ca2+ current is subject to resting inhibition by G proteins.

Original languageEnglish (US)
Pages (from-to)72-77
Number of pages6
JournalPflügers Archiv European Journal of Physiology
Issue number1
StatePublished - Jan 1 1992


  • Ca channels
  • G proteins
  • Insulin secretion
  • Pancreatic β cells

ASJC Scopus subject areas

  • Physiology


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