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Advancing Age Alters the Contribution of Calcium Release From Smooth Endoplasmic Reticulum Stores in Superior Cervical Ganglion Cells

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)...

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Detalles Bibliográficos
Autores principales: Behringer, Erik J., Vanterpool, Conwin K., Pearce, William J., Wilson, Sean M., Buchholz, John N.
Formato: Texto
Lenguaje:English
Publicado: Oxford University Press 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673896/
https://www.ncbi.nlm.nih.gov/pubmed/19196634
http://dx.doi.org/10.1093/gerona/gln053
Descripción
Sumario: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.