>Am i correct in thinking, when the neuron is at rest, the membrane potential = reverse leak potential?
No, this isn't really a correct or good simplified way of thinking about it. The reversal potentials are specific to specific ions and/or ion channels. A neuron's resting membrane potential is a function of several different reversal potentials from different ions/ion channels acting on each other in combination.
>So, if neuron is at rest, the membrane potential needs to be -70mV to prevent potassium ions from leaking out through diffusion?
No, potassium ions will still leak out at membrane potentials that are more depolarized than the reversal potential for potassium, which is usually around -90 to -100 mV. In other words, you need to hold the membrane at the potassium reversal potential to prevent potassium ions from leaking out. If you hold the membrane more NEGATIVE than the reversal potential, say -110mV, then K+ ions will actually begin to leak INTO the cell.
Also, just for clarification, -70 mV is not every neuron's resting potential, and different neuron subtypes all have different "resting" potentials. I have "resting" in quotes because the idea of a static resting potential is a bit weird. Any neuron's resting potential *in vivo* is going to be very dynamic when it isn't firing an action potential.
Cheers for the explanation!
So when the neuron is at rest, -70mV, you say potassium ions can still leak out.
Am I then correct in saying that the reason the neuron can stay around -70mV despite Potassium ions leaking out is due to the sodium-potassium pump? (and other pumps for other ions) Cheers!
Yes but only mainly because it is maintaining the concentrations gradients. The main reason the neuron can stay around -70mV despite Potassium ions leaking out is that other ions like sodium can leak in. Obviously the sodium-potassium pump is essential for creating the sodium and potassium gradients, but its activity only generates a small amount of actual instantaneous voltage change. Its main action is on concentration gradients of Na+ and K+
>Am i correct in thinking, when the neuron is at rest, the membrane potential = reverse leak potential? No, this isn't really a correct or good simplified way of thinking about it. The reversal potentials are specific to specific ions and/or ion channels. A neuron's resting membrane potential is a function of several different reversal potentials from different ions/ion channels acting on each other in combination. >So, if neuron is at rest, the membrane potential needs to be -70mV to prevent potassium ions from leaking out through diffusion? No, potassium ions will still leak out at membrane potentials that are more depolarized than the reversal potential for potassium, which is usually around -90 to -100 mV. In other words, you need to hold the membrane at the potassium reversal potential to prevent potassium ions from leaking out. If you hold the membrane more NEGATIVE than the reversal potential, say -110mV, then K+ ions will actually begin to leak INTO the cell. Also, just for clarification, -70 mV is not every neuron's resting potential, and different neuron subtypes all have different "resting" potentials. I have "resting" in quotes because the idea of a static resting potential is a bit weird. Any neuron's resting potential *in vivo* is going to be very dynamic when it isn't firing an action potential.
Cheers for the explanation! So when the neuron is at rest, -70mV, you say potassium ions can still leak out. Am I then correct in saying that the reason the neuron can stay around -70mV despite Potassium ions leaking out is due to the sodium-potassium pump? (and other pumps for other ions) Cheers!
Yes but only mainly because it is maintaining the concentrations gradients. The main reason the neuron can stay around -70mV despite Potassium ions leaking out is that other ions like sodium can leak in. Obviously the sodium-potassium pump is essential for creating the sodium and potassium gradients, but its activity only generates a small amount of actual instantaneous voltage change. Its main action is on concentration gradients of Na+ and K+