Carlson A D, Treherne J E
J Exp Biol. 1977 Apr;67:205-15. doi: 10.1242/jeb.67.1.205.
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.
尽管这种海洋渗透压顺应者的血液浓度会出现极大波动,但在等渗条件下,巨轴突传导基本上涉及“传统的”离子机制。静息轴突膜近似于一个理想的钾电极,在[K⁺]O高于10 mM时,[K⁺]O每变化十倍,斜率为58 - 8 mV。动作电位的超射值随着[Na⁺]O每降低十倍下降55 - 8 mV,并且动作电位在约5×10⁻⁷ M的河豚毒素作用下被阻断。在高达血液中发现的相对较高水平30 mM的钾浓度下,动作电位的上升相和超射值保持恒定,这表明在广泛的静息电位范围内,钠失活异常缺失。从[K⁺]O变化引起的电位变化可以推断,钾离子在浸泡介质和轴突表面之间相对快速、对称地移动。钠离子的外向移动(t₀₋₅ = 33 - 5 s)与钾离子的移动速率相似,但钠离子的内向移动相对缓慢且复杂。可以得出结论,轴突在稀释介质中发挥功能的能力必定涉及对渗透压和离子应激的特定适应性变化。