Action potential changes in low sodium concentrations but constant osmotic pressure

Question

If I bathe a squid axon in a fluid that has high sodium concentration , why does the duration of action potential decrease compared to a control experiment in low sodium bath but maintained at the same osmotic pressure with choline chloride? Why does the amplitude of action potential increase in the experimental set ?

In short- In the experiment, when the neurons are bathed in low sodium fluid but constant osmotic pressure, amplitude of action potential decreased, but duration of action potential increased.

I wanted to validate this with Nernst equation and/or GHK equation .

The increase is action potential amplitude with high extracellular sodium ( more sodium influx,more depolarization ? ) is intuitive? But again I am confused because the membrane is only slightly permeable to sodium such that increases in extracellular sodium won't really alter the membrane potential enough to generate an action potential.

Also how does the action potential duration decrease in high sodium ?

What should be done if I want to increase duration of action potential while keeping the axons in high sodium bath ?

1. The duration of action potential is not the time to reach threshold voltage. It is the overall time the membrane stays depolarized.
2. In other words, why are the axons slowly repolarized when bathed in low sodium concentration(and also maintained at constant osmotic pressure with choline chloride ) compared to high sodium bath axons that are rapidly repolarized ?

How do you think the answer would've changed if choline chloride was not used ?

Answer 1

High sodium extracellularly means an increased sodium concentration gradient across the membrane. This means there is a larger driving force for sodium to enter the cell once the sodium channels open at the start of the action potential, and hence a larger depolarization takes place increasing the action potential amplitude. The enhanced depolarization leads to an increased proportion of activated voltage-operated potassium channels that open upon depolarization. When more potassium channels open, more potassium will exit the cell, thereby repolarizing the cell to a larger extent, in turn stopping the depolarization step of the action potential faster. In all, the action potential develops quicker, as the depolarization is increased as well as the repolarization step, and hence the time it takes to execute an action potential is diminished.

Your subquestion as to the small sodium conductance is not valid, as during an action potential it is actually very high.

To increase the action potential duration you can increase the re-polarization step by increasing the extracellular potassium concentration, thereby diminishing the potassium concentration gradient and prolonging the repolarization step.

Answer 2

Not different from @ChrisStronks answer. Just in different words.

Just for everyone's knowledge — you are referring to the Voltage-clamp experiment.

Situation 1: Sodium is depleted in the ECF.

Despite the fact that Na⁺ conductance is much less than that of K⁺ and the equilibrium membrane potential (hyperpolarized) is closer to Nernst potential of K⁺, absence of Na⁺ would move the equilibrium potential closer to the K⁺ Nernst potential. This would result in increase in the response time of action potential (AP).

Situation 2: Sodium is increased in the ECF

The consequence of this would depend on how much is the concentration of Na⁺. You can calculate the changed Nerst potential of Na⁺ using the Nernst-Plank equation.
How would it decrease the response time of AP?
It would increase Nernst potential of Na⁺ causing an increase in the sodium current. This would increase the rate of AP and therefore decrease the response time.