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Cyclic ADP‐ribose induced Ca 2+ release in rabbit skeletal muscle sarcoplasmic reticulum
Author(s) -
Morrissette Jeffery,
Heisermann Gary,
Cleary John,
Ruoho Arnold,
Coronado Roberto
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)80886-y
Subject(s) - ruthenium red , ryanodine receptor , cyclic adp ribose , endoplasmic reticulum , skeletal muscle , metabolite , chemistry , biophysics , ryanodine receptor 2 , biochemistry , calcium , endocrinology , biology , microbiology and biotechnology , cd38 , stem cell , organic chemistry , cd34
The Ca 2+ ‐mobilizing metabolite cyclic ADP‐ribose (cADPR) has been shown to release Ca 2+ from ryanodine‐sensitive stores in many cells. We show that this metabolite at a concentration of 17μM, but not its precursor β‐NAD + nor non‐cyclic ADPR at the same concentration, is active in releasing Ca 2+ from rabbit skeletal muscle sarcoplasmic reticulum. The release was not sensitive to Ruthenium red (1μM) nor to the ryanodine receptor‐specific scorpion toxin Buthotus 1 ‐1 (10 μM). In planar bilayer single channel recordings, concentrations up to 50μM cADPR did not increase the open probability of Ruthenium red and toxin‐sensitive Ca 2+ release channels. Thus Ca 2+ release induced by cADPR in skeletal muscle sarcoplasmic reticulum may not involve opening of ryanodine receptors.