In superior cervical ganglion (SCG) neurons calcium-induced calcium release (CICR), mediated by ryanodine receptors (RyRs), contributes to stimulation-evoked intracellular calcium ([Ca(2+)](i)) transients. Hypothesis: The contribution of CICR to electrical field stimulation (EFS)-evoked [Ca(2+)](i) transients in SCG cells declines with senescence and may be partially recovered in the presence of caffeine. We measured EFS-evoked [Ca(2+)](i) 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+)](i) transients or caffeine to sensitize CICR to EFS. EFS-evoked [Ca(2+)](i) transients increased from 6 to 12 months and declined at 24 months and ryanodine decreased [Ca(2+)](i) transients in SCG cells from 6- and 12-month-old animals only. Caffeine significantly increased EFS-evoked [Ca(2+)](i) 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.
展开▼
