年龄增长会改变颈上神经节细胞中滑面内质网钙库释放钙的作用。
Advancing age alters the contribution of calcium release from smooth endoplasmic reticulum stores in superior cervical ganglion cells.
作者信息
Behringer Erik J, Vanterpool Conwin K, Pearce William J, Wilson Sean M, Buchholz John N
机构信息
Department of Physiology and Pharmacology, Loma Linda University, CA 92354, USA.
出版信息
J Gerontol A Biol Sci Med Sci. 2009 Jan;64(1):34-44. doi: 10.1093/gerona/gln053. Epub 2009 Feb 4.
UNLABELLED
In superior cervical ganglion (SCG) neurons calcium-induced calcium release (CICR), mediated by ryanodine receptors (RyRs), contributes to stimulation-evoked intracellular calcium (Ca(2+)) transients.
HYPOTHESIS
The contribution of CICR to electrical field stimulation (EFS)-evoked Ca(2+) transients in SCG cells declines with senescence and may be partially recovered in the presence of caffeine. We measured EFS-evoked Ca(2+) transients in isolated fura-2-loaded SCG cells from Fischer-344 rats aged 6, 12, and 24 months with either the RyR antagonist ryanodine to block the contribution of CICR to Ca(2+) transients or caffeine to sensitize CICR to EFS. EFS-evoked Ca(2+) transients increased from 6 to 12 months and declined at 24 months and ryanodine decreased Ca(2+) transients in SCG cells from 6- and 12-month-old animals only. Caffeine significantly increased EFS-evoked Ca(2+) transients in all age groups. These data suggest that CICR declines with senescence and residual CICR function may be reclaimed in senescent cells with caffeine.
未标记
在颈上神经节（SCG）神经元中，由兰尼碱受体（RyRs）介导的钙诱导钙释放（CICR）有助于刺激诱发的细胞内钙（Ca(2+)）瞬变。
假设
CICR对SCG细胞中电场刺激（EFS）诱发的Ca(2+)瞬变的贡献随衰老而下降，并且在咖啡因存在的情况下可能部分恢复。我们用RyR拮抗剂兰尼碱阻断CICR对Ca(2+)瞬变的贡献，或用咖啡因使CICR对EFS敏感，测量了来自6、12和24月龄Fischer-344大鼠的分离的负载fura-2的SCG细胞中EFS诱发的Ca(2+)瞬变。EFS诱发的Ca(2+)瞬变从6个月到12个月增加，在24个月时下降，并且兰尼碱仅降低了6月龄和12月龄动物的SCG细胞中的Ca(2+)瞬变。咖啡因在所有年龄组中均显著增加了EFS诱发的Ca(2+)瞬变。这些数据表明，CICR随衰老而下降，并且衰老细胞中残留的CICR功能可能通过咖啡因恢复。
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