Ca2+ release induced by cyclic ADP ribose in mice lacking type 3 ryanodine receptor

Biochem Biophys Res Commun. 2001 Nov 2;288(3):697-702. doi: 10.1006/bbrc.2001.5834.

Abstract

The action of cyclic-ADP-ribose was studied on calcium release from sarcoplasmic reticulum of skeletal muscles of neonatal and adult wild-type and RyR3-deficient mice. cADPR increased calcium efflux from microsomes, enhanced caffeine-induced calcium release, and, in 20% of the tests, triggered calcium release in single muscle fibers. These responses occurred only in the diaphragm of adult RyR3-deficient mice. cADPR action was abolished by ryanodine, ruthenium red, and 8-brome-cADPR. These results strongly favor a specific action of cADPR on RyR1. The responsiveness of RyR1 appears in adult muscles when RyR3 is lacking.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Diphosphate Ribose / analogs & derivatives*
  • Adenosine Diphosphate Ribose / pharmacology*
  • Animals
  • Calcium / metabolism*
  • Cyclic ADP-Ribose
  • Mice
  • Mice, Knockout
  • Microsomes / drug effects
  • Microsomes / metabolism
  • Muscle Fibers, Skeletal / drug effects*
  • Muscle Fibers, Skeletal / metabolism
  • Permeability
  • Ryanodine Receptor Calcium Release Channel / deficiency
  • Ryanodine Receptor Calcium Release Channel / genetics
  • Ryanodine Receptor Calcium Release Channel / metabolism*

Substances

  • Ryanodine Receptor Calcium Release Channel
  • Cyclic ADP-Ribose
  • Adenosine Diphosphate Ribose
  • Calcium

Grants and funding