The control of ionized calcium in squid axons.
Measurements of the Ca content, [Ca](T), of freshly isolated squid axons show a value of 60 mumol/kg axoplasm. Axons in 3 mM Ca(Na) seawater show little change in Ca content over 4 h, while axons in 3 mM Ca(Na) seawater show little change in Ca content over 4 h, while axons in 10 mM Ca(Na) seawater show gains of 18 mumol/Ca/kgxh. In 10 Ca (Choline) seawater the gain is 2,400 mumol/kgxh. Using aequorin confined to a dialysis capillary in the center of an axon, one finds that [Ca](i) is in a steady state with 3 Ca (Na) seawater, and that both 10 Ca (Na) and 3 Ca (choline) seawater cause increases in [Ca](i). In 3 Ca (Na) seawater-3 Ca (choline) seawater mixtures, 180 mM [Na](0) (40 perecent Na) is as effective as 450 mM [Na](0) (100 percent Na) in maintaining a normal [Ca](1); lower [Na] causes an increase in [Ca](i). If axons are injected with the ATP-splitting enzyme apyrase, the resulting [Ca](1) is not loading with high [Ca](0) or low [Na](0) solutions. Depolarization of an axon with 100 mM K (Na) seawater leads to an increase in the steady-state level of [Ca](1) that is reversed upon returning the axon to normal seawater. Freshly isolated axons treated with either CN or FCCP to inhibit mitochondrial Ca buffering can still maintain a normal [Ca](i) in 1 Ca (Na) seawater.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000331:Aequorin / Q000494:pharmacology; D000818:Animals; D001081:Apyrase / Q000494:pharmacology; D001369:Axons / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002463:Cell Membrane Permeability / Q000187:drug effects; D002794:Choline / Q000494:pharmacology; D049832:Decapodiformes / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects; D008928:Mitochondria / Q000378:metabolism; D009994:Osmolar Concentration; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology
D000331:Aequorin; D000255:Adenosine Triphosphate; D012964:Sodium; D001081:Apyrase; D002794:Choline; D002118:Calcium