Despite the extreme fluctuations in blood concentration experienced by this marine osmoconformer, essentially ‘conventional’ ionic mechanisms are involved in conduction by the giant axons in isosmotic conditions. The resting axonal membrane approximates to an ideal potassium electrode, with a 58-8 mV slope for decade change in [K+]O above 10 mM. The action potential overshoot shows a 55-8 mV decline with decade reduction in [Na+]O and the action potentials are blocked by tetrodotoxin at around 5 X 10(−7) M. The rising phase and overshoot of the action potential remain constant at potassium concentrations up to the relatively high level of 30 mM found in the blood, indicating an unusual absence of sodium inactivation over a wide range of resting potentials. Relatively rapid, symmetrical movement of potassium ions between the bathing medium and the axon surface is deduced from the potential changes induced by alterations in [K+]O. Outward movement of sodium ions (t0-5 = 33-5 s) occurs at a similar rate to that of potassium, but inward movement of Na+ is relatively slow and complex. It is concluded that the ability of axons to function in dilute media must involve specific adaptations to osmotic and ionic stress.

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