Modulation of IP3-sensitive Ca2+ release by 2,3-butanedione monoxime

• Published in: Pflügers Archiv 2003-02, Vol.445 (5), p.614-621
• Main Authors: Turvey, Matthew R., Laude, Alex J., Ives, E. Oliver H., Seager, William H., Taylor, Colin W., Thorn, Peter
• Format: Article
• Language: English
• ISSN: 0031-6768; 1432-2013
• DOI: 10.1007/s00424-002-0984-9

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^sub 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^sub 3^ receptors.[PUBLICATION ABSTRACT]