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Measurement of Calcium Fluctuations Within the Sarcoplasmic Reticulum of Cultured Smooth Muscle Cells Using FRET-based Confocal Imaging
Published on: June 20, 2016
Cytoplasmic Ca2+ activity regulation as measured by a calcium-activated current
1Department of Physiology, University of New Mexico, Albuquerque 87131.
Brain Research
|May 30, 1994
Summary
Mitochondria are crucial for regulating calcium-activated non-selective cation (CAN) currents in snail neurons. Blocking mitochondrial calcium uptake significantly slowed CAN current decay, highlighting their role as the primary calcium sink.
Area of Science:
- Neuroscience
- Cell Physiology
- Ion Channel Function
Background:
- Calcium-activated non-selective cation (CAN) currents play a role in neuronal excitability.
- Understanding the regulation of intracellular calcium (Ca2+) is vital for neuronal function.
- The specific cellular compartments responsible for buffering sub-membrane Ca2+ remain incompletely understood.
Purpose of the Study:
- To investigate the role of cellular organelles in buffering sub-membrane Ca2+ during the activation of CAN currents.
- To identify the primary cellular sink for Ca2+ that regulates CAN current kinetics.
Main Methods:
- Quantitative Ca2+ injections into voltage-clamped bursting neurons from Helix aspersa or Helix pomatia.
- Selective pharmacological blockade of Ca2+ transporters and pumps in the cell membrane, endoplasmic reticulum, and mitochondria.
- Measurement and kinetic analysis (rising and falling exponential function) of CAN currents.
- Assessment of the effects of various agents (0 Na Ringers, chlorpromazine, Na3VO4, thapsigargin, 2,4-dinitrophenol, ruthenium red) on CAN current decay.
Main Results:
- Pharmacological agents targeting the cell membrane, endoplasmic reticulum, and mitochondria (except for 2,4-dinitrophenol and ruthenium red) did not significantly alter CAN current decay constants.
- External 2,4-dinitrophenol and internal ruthenium red significantly lengthened the CAN current decay constant.
- These findings indicate a critical role for mitochondria in Ca2+ buffering.
Conclusions:
- Mitochondria serve as the most significant sink for sub-membrane Ca2+ activity in the physiological range required for CAN current activation.
- The study elucidates the crucial role of mitochondria in regulating neuronal excitability through calcium buffering.
- These findings contribute to a deeper understanding of calcium dynamics in neurons.
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