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Related Experiment Videos

Cyclic ADP-ribose-induced Ca2+ release from rat brain microsomes

A M White1, S P Watson, A Galione

  • 1Department of Pharmacology, University of Oxford, UK.

FEBS Letters
|March 8, 1993
PubMed
Summary

Cyclic ADP-ribose (cADPR) triggers calcium release from rat brain microsomes. This calcium signaling is mediated by ryanodine-sensitive channels, distinct from IP3 pathways.

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Area of Science:

  • Biochemistry
  • Cellular Physiology
  • Neuroscience

Background:

  • Cyclic ADP-ribose (cADPR) is an endogenous metabolite of NAD+.
  • cADPR is known to mobilize calcium in various tissues, including sea urchin eggs.
  • The role of cADPR in mammalian brain calcium signaling remains less understood.

Purpose of the Study:

  • To investigate the effect of cADPR on calcium release from mammalian brain microsomes.
  • To determine the concentration-dependent effects of cADPR on calcium mobilization.
  • To elucidate the specific calcium channels involved in cADPR-mediated calcium release in the brain.

Main Methods:

  • Preparation of rat brain microsomes.
  • Measurement of calcium release in response to varying concentrations of cADPR.
  • Assessment of the effects of heparin and ryanodine on cADPR-induced calcium release.

Main Results:

  • cADPR stimulates significant calcium release from rat brain microsomes within the 10-250 nM concentration range.
  • Heparin, an inhibitor of inositol 1,4,5-trisphosphate (IP3)-induced calcium release, did not affect cADPR-mediated release.
  • Ryanodine, a known modulator of ryanodine receptors, inhibited cADPR-induced calcium release.

Conclusions:

  • cADPR acts as a calcium-mobilizing messenger in the mammalian brain.
  • The calcium pools sensitive to cADPR in the brain appear to be ryanodine-sensitive.
  • These findings suggest a novel role for cADPR in regulating intracellular calcium dynamics in neuronal tissues, distinct from IP3 signaling pathways.

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