Medical Why Does Permeability Alter Membrane Potential?

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Changes in membrane permeability directly influence membrane potential due to the dynamics of ion movement across the membrane. The Goldman-Hodgkin-Katz (GHK) equation allows for the calculation of membrane potential by considering the concentration gradients and permeabilities of various ions, resulting in a weighted average of their equilibrium potentials. While it may seem that changes in permeability should only gradually shift the membrane potential toward equilibrium, the opening of voltage-gated channels facilitates rapid changes. This process occurs because multiple channels open in succession along the axon, allowing for immediate current influx, which is faster than classical diffusion of charged particles. Experimental observations, such as measuring sodium transport across epithelial tissue, further illustrate these principles, demonstrating significant voltage changes in response to alterations in ion channel activity within seconds.
horsecandy911
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I've just finished reading through the generally well-written Wikipedia article on membrane potential:

http://en.wikipedia.org/wiki/Membrane_potential

I found almost everything to be clear, but one question is nagging at me. Why do changes in membrane permeability directly affect membrane potential? The Wikipedia article says:

The more ions are permeant, the more complicated it becomes to predict the membrane potential. However, this can be done using the Goldman-Hodgkin-Katz equation or the weighted means equation. By simply plugging in the concentration gradients and the permeabilities of the ions at any instant in time, one can determine the membrane potential at that moment. What the GHK equations says, basically, is that at any time, the value of the membrane potential will be a weighted average of the equilibrium potentials of all permeant ions. The "weighting" is the ions relative permeability across the membrane.

I can understand why membrane permeabilities affect the equilibrium potential, but why should they affect the membrane potential instantaneously? Isn't the potential totally determined by the concentrations of charge inside and outside the membrane? Changing permeabilities by opening ion channels should shift the equilibrium potential and cause a gradual change in membrane potential in the direction of equilibrium, but they should not change the membrane potential immediately. Am I misunderstanding something? Thanks.
 
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horsecandy911 said:
Changing permeabilities by opening ion channels should shift the equilibrium potential and cause a gradual change in membrane potential in the direction of equilibrium, but they should not change the membrane potential immediately.


"Immediately" is a relative term. Voltage-gated channels do not require us to wait on the charged particles to spread down the axon. Instead, we have a lot of channels open up in series down the axon and at each a point, a new current comes into the axon through its own gate. So no, it's not immediate, but it's faster than if the charged particles only diffused classically down the axon (much faster).
 
horsecandy911 said:
I can understand why membrane permeabilities affect the equilibrium potential, but why should they affect the membrane potential instantaneously? Isn't the potential totally determined by the concentrations of charge inside and outside the membrane? Changing permeabilities by opening ion channels should shift the equilibrium potential and cause a gradual change in membrane potential in the direction of equilibrium, but they should not change the membrane potential immediately. Am I misunderstanding something? Thanks.

I use sodium transport as an experimental readout by measuring the equivalent short-circuit current across a sample of epithelial tissue, and this is due to an apical sodium channel (ENaC) and a few baso-lateral transporters (Na-K-ATPase and RomK) which result in a vectoral transport of sodium.

I can verify that the measured voltage is in fact due to sodium transport (as opposed to some other ion) by plugging ENaC with amiloride. The transepithelial current drops by 90% over a period of seconds when this happens, which should give you an idea of the timescale.
 
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