Effects of Altered Extracellular Ion Concentrations on Resting Membrane Potentials, Action Potentials, and Excitability Flashcards
As the ratio of ion concentrations inside and outside the cell approaches one
Nernst potential approaches 0 because log(1)=0
you substitute the new Nernst value into the MCC equation whil ekeeping permability ratios the same in order to
calculate the new resting membran epotential
How does lowering external [Na+] affect
- peak amplitude
- duration of the action potential
- resting membrane potential
Decreases amplitude
Increases duration (slower)
Basically no change in the RMP
Decreasing extracellular [Na+] __creases teh value of ENa
Decreases - the action potential is a lower value
Why is the action potential affected more by decreasing extracellular Na than the resting membrane potential?
The permeability of the membrane to Na+ is much greater during the action potential than at rest
The __ Nernst potential is the most influential one contributing to Em because ____
The K Nernst potential is most influential becuase PK > PNa
As extracellular K+ increases, this causes a progressive depolarization of Ek, which causes depolarization of Em
The biphasic effect of graded depolarization (progressively increasing [K+]out) on membrane excitability
Mild/moderate depolarization will increase excitability, but stronger depolarization decreases excitability. Even stronger depolarization will block action potentials altogether.
Graded depolarization of K (progressively increasing [K+]out) has what impact on action potential amplitudes?
WHY?
Decreases peak amplitudes
Because it increases the fraction of Na channels that are inactivated.
Why does depolarization/increasing the resting membrane potential cause smaller and slower action potentials?
It increases the number of Na channels activated but also increases the fraction that are inactivated and thus unavailable to open when threshold is reached.
Effect of [Ca2+]out on threshold and excitability
Why does increasing [Ca2+]out increase the threshold for action potentials?
- Ca2+ competes with Na2+ for sites in the sodium channel –> less sodium can enter to elicit an action potential
- Ca2+ screens fixed negative charges on the outside of the cell membane, which alters the magnitude of the local electrical field acting on the ion gates
What channel is progressively being blocked off in this action potential?
Na channels are being blocked with increasing concentrations of tetrodotoxin, revealing the later, prolonged Ca2+ component of the action potential
The increase in [Ca2+]in during an action potential has what impact on K+ efflux?
Just like Na, as Ca2+ enters, it can trigger outward K+ flux to terminate the burst of action potential
One important role for Cl- channels across the cell membrane is
inhibitory synpatic potentials
Two reasons why we don’t worry about excessive Na accumulating inside and losing too much K
1) The total number of Na+ that has to enter to produce the depolarization of an AP is very small and the number of K+ needed to leave to produce repolarize is very small
2) Na-K pump replenishes any intracellular K+ loss and extrudes the accumulated Na+ in seconds