Advancing age alters the contribution of calcium release from smooth endoplasmic reticulum stores in superior cervical ganglion cells

Research output: Contribution to journalArticlepeer-review

Abstract

In superior cervical ganglion (SCG) neurons calcium-induced calcium release (CICR), mediated by ryanodine receptors (RyRs), contributes to stimulation-evoked intracellular calcium ([Ca2+]i) transients. Hypothesis: The contribution of CICR to electrical field stimulation (EFS)-evoked [Ca2+]i transients in SCG cells declines with senescence and may be partially recovered in the presence of caffeine. We measured EFS-evoked [Ca2+]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 [Ca2+]i transients or caffeine to sensitize CICR to EFS. EFS-evoked [Ca2+]i transients increased from 6 to 12 months and declined at 24 months and ryanodine decreased [Ca2+] i transients in SCG cells from 6- and 12-month-old animals only. Caffeine significantly increased EFS-evoked [Ca2+]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. © 2009 The Author(s).
Original languageEnglish
Pages (from-to)34-44
Number of pages11
JournalJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Volume64
Issue number1
DOIs
StatePublished - Jan 2009

ASJC Scopus Subject Areas

  • Aging
  • Geriatrics and Gerontology

Keywords

  • Aging and calcium release
  • Aging and function of superior cervical ganglia
  • Ryanodine receptors
  • Caffeine/pharmacology
  • Aging/metabolism
  • Electric Stimulation
  • Rats, Inbred F344
  • Muscle, Smooth/cytology
  • Rats
  • Ryanodine Receptor Calcium Release Channel/drug effects
  • Male
  • Ryanodine/pharmacology
  • Calcium/metabolism
  • Animals
  • Superior Cervical Ganglion/cytology
  • Intracellular Fluid/metabolism
  • Membrane Potentials/drug effects
  • Endoplasmic Reticulum/metabolism

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