环磷酸腺苷核糖诱导大鼠脑微粒体释放钙离子。
Cyclic ADP-ribose-induced Ca2+ release from rat brain microsomes.
作者信息
White A M, Watson S P, Galione A
机构信息
Department of Pharmacology, University of Oxford, UK.
出版信息
FEBS Lett. 1993 Mar 8;318(3):259-63. doi: 10.1016/0014-5793(93)80524-x.
Cyclic ADP-ribose (cADPR), an endogenous NAD+ metabolite in many mammalian and invertebrate tissues, is a potent mediator of calcium mobilization in sea urchin eggs. Our results show that cADPR also stimulates calcium release from rat brain microsomes, marked release occurring over the concentration range 10-250 nM. This is not inhibited by concentrations of heparin which completely abolish inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release. Ryanodine (100 microM) inhibits the cADPR response. Our results are consistent with cADPR being an endogenous messenger mediating Ca2+ release from ryanodine-sensitive pools in brain.
环磷酸腺苷核糖（cADPR）是许多哺乳动物和无脊椎动物组织中的一种内源性烟酰胺腺嘌呤二核苷酸（NAD+）代谢产物，是海胆卵中钙动员的有效介质。我们的结果表明，cADPR还能刺激大鼠脑微粒体释放钙，在10 - 250 nM的浓度范围内有明显的释放。这种释放不受肝素浓度的抑制，而肝素能完全消除肌醇1,4,5 - 三磷酸（IP3）诱导的Ca2+释放。Ryanodine（100 microM）抑制cADPR反应。我们的结果与cADPR作为一种内源性信使介导脑内ryanodine敏感池释放Ca2+一致。
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