Reversible blockade of gap junctional communication by 2, 3
-butanedione monoxime (bdm) in rat cardiac myocytes.
Verrecchia, F., and J. C. Herv[acute]e.
Laboratoire de Physiologie Cellulaire, Unit[acute]e de Recherche
Associ[acute]ee au CNRS n degrees 1869, 40, avenue du R. Pineau,
86022 Poitiers, France
APStracts 3:0340C, 1996.
2,3 butanedione monoxime (BDM), a nucleophilic agent endowed with a
"phosphatase-like" activity, is often used as a tool for
investigating the effects of changes in phosphorylation level of
protein constituents on membrane channel function. BDM produced a
rapid, dose-dependent and reversible abolition of the cytosolic
continuity existing between cells via gap junctional channels. The
persistence of this effect when a non-hydrolysable analogue of
adenosine 5'-triphosphate (ATPS) was introduced in the cytosol
suggests that the acute suppressant effect of BDM was not due to
dephosphorylation. However, the higher reversibility after BDM
withdrawal in presence of ATPS could signify that a protein
dephosphorylating activity gradually occurred during the oxime
treatment. Junctional uncoupling took place even when the moderate
increase in cytosolic calcium concentration induced by BDM was
prevented by ryanodine. These results are consistent with the model
of dual mechanism of BDM action proposed for some other membrane
channels, consisting of a quick channel block and a parallel slow
inhibition, plausibly through dephosphorylation.
Received 29 July 1996; accepted in final form 23 October 1996.
APS Manuscript Number C422-6.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996