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Quantitative estimate of mitochondrial [Ca2+] in stimulated motor nerve terminals

Gavriel David1, Janet Talbot, Ellen F Barrett

  • 1Department of Physiology and Biophysics, University of Miami School of Medicine, R-430, P.O. Box 016430, Miami, FL 33101, USA. gdavid@newssun.med.miami.edu

Cell Calcium
|February 26, 2003
PubMed

Insights

Mitochondrial matrix calcium levels in lizard motor terminals were measured using a low-affinity dye, revealing a stable plateau of approximately 1 microM during stimulation. This indicates a potent mitochondrial calcium buffering system, unaffected by changes in calcium influx or stimulation frequency.

Area of Science:

  • Cellular Biology
  • Neuroscience
  • Mitochondrial Physiology

Background:

  • Mitochondrial matrix calcium ([Ca(2+)]) measurements vary widely, from micromolar to millimolar.
  • High-affinity fluorescent dyes risk saturation at high calcium concentrations, potentially skewing results.

Purpose of the Study:

  • To accurately measure mitochondrial matrix calcium during stimulation in lizard motor terminals.
  • To investigate the buffering capacity of mitochondria under varying calcium loads.

Main Methods:

  • Utilized the low-affinity fluorescent indicator rhod-5N (K(d) ≈ 320 µM) to avoid dye saturation.
  • Stimulated lizard motor terminals with action potentials at 50Hz.
  • Manipulated extracellular calcium and used 3,4-diaminopyridine to alter calcium influx.

Main Results:

  • Matrix calcium fluorescence reached a stable plateau during 50Hz stimulation, irrespective of altered calcium entry.
  • The plateau level corresponded to approximately 1 µM matrix calcium, confirmed by calculations.
  • This stable plateau persisted even when stimulation frequency or calcium influx was modified.

Conclusions:

  • Lizard motor terminal mitochondria possess a powerful endogenous calcium buffering mechanism.
  • The buffering system maintains matrix calcium at a stable ~1 µM level, preventing saturation of low-affinity indicators.
  • This buffering is a critical factor in regulating mitochondrial function during neuronal activity.

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