Modulation of IP(3)-sensitive Ca(2+) release by 2,3-butanedione monoxime

Pflugers Arch. 2003 Feb;445(5):614-21. doi: 10.1007/s00424-002-0984-9. Epub 2002 Dec 6.


We describe the actions of 2,3-butanedione monoxime (BDM) on calcium responses in secretory cells. Our studies were prompted by the widespread use of BDM as a myosin-ATPase inhibitor. Application of 10 mM BDM almost completely inhibited agonist-evoked amylase secretion from mouse pancreatic acinar cells. This action might be interpreted as indicating a role for myosin in secretion. However, BDM alone elicited a calcium response in single cells and this calcium signal was sufficient to activate calcium-dependent chloride currents. Furthermore, in some cases, BDM potentiated agonist-evoked calcium signals but almost always blocked agonist-evoked calcium oscillations. These effects of BDM were not due to an action on calcium influx pathways but rather to direct effects on IP(3)-sensitive stores. We conclude that BDM cannot be used for unequivocal identification of the involvement of myosin motors in a cellular response. Further, our evidence suggests that BDM can act directly to modify the opening of IP(3) receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / pharmacology
  • Animals
  • Animals, Outbred Strains
  • Calcium / metabolism*
  • Calcium / physiology
  • Diacetyl / analogs & derivatives*
  • Diacetyl / pharmacology*
  • Electrophysiology
  • Enzyme Inhibitors / pharmacology*
  • Inositol 1,4,5-Trisphosphate / physiology*
  • Intracellular Membranes / metabolism
  • Male
  • Mice
  • Myosins / antagonists & inhibitors
  • Oscillometry
  • Osmolar Concentration
  • Pancreas / cytology
  • Pancreas / drug effects
  • Pancreas / metabolism*
  • Patch-Clamp Techniques


  • Enzyme Inhibitors
  • diacetylmonoxime
  • Inositol 1,4,5-Trisphosphate
  • Myosins
  • Diacetyl
  • Acetylcholine
  • Calcium