Cytoplasmic Ca2+ activity regulation as measured by a calcium-activated current

Calcium-activated non-selective cation (CAN) currents were activated by quantitative injections of Ca2+ into voltage clamped bursting neurons of the snails Helix aspersa or Helix pomatia. Membrane potential was held at the potassium equilibrium potential and CAN currents were fit with a rising and falling exponential function. Ca2+ transporters and pumps of the cell membrane, endoplasmic reticulum, and mitochondria were selectively blocked with pharmacological agents. Bath solutions containing 0 Na Ringers, chlorpromazine, Na3VO4, or thapsigargin did not significantly change the CAN current decay constants from those measured in Ringers. External 2,4-dinitrophenol or internal ruthenium red, however, significantly lengthened the CAN current decay constant. It is concluded that mitochondria are the most important sink for sub-membrane Ca2+ activity in the range necessary to effectively activate CAN currents.