| Abstract: | Measurements of the Ca content, Ca](T), of freshly isolated squid axons show a value of 60 μmol/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 μmol/Ca/kgxh. In 10 Ca (Choline) seawater the gain is 2,400 μmol/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. |
