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.
Partridge
L D
LD
Department of Physiology, University of New Mexico, Albuquerque 87131.
D019297:2,4-Dinitrophenol; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism* / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002746:Chlorpromazine / Q000494:pharmacology; D003593:Cytoplasm / Q000378:metabolism*; D004140:Dinitrophenols / Q000494:pharmacology; D004594:Electrophysiology; D006372:Helix, Snails; D008928:Mitochondria / Q000378:metabolism; D009474:Neurons / Q000378:metabolism* / Q000502:physiology; D012430:Ruthenium Red / Q000494:pharmacology
D002121:Calcium Channel Blockers; D004140:Dinitrophenols; D012430:Ruthenium Red; D019297:2,4-Dinitrophenol; D002118:Calcium; D002746:Chlorpromazine