L/D 2: Membrane & Action Potentials Flashcards
what does a negative membrane potential signify? which direction is the force on cations? anions?
inside is lower potential than outside
force on cations is inward
force on anions is outward
what does a positive membrane potential signify? which direction is the force on cations? anions?
inside is higher potential than outside
force on cations is outward
force on anions is inward
[K+] in = 100 mEq/L
[K+] out = 10 mEq/L
and K+ is at equilibrium distribution,
what is Vm?
Vm = Ek = -61log(100/10)
= -61 mV
If you know Vm and various in vs out ion concentrations of a cell membrane, how do you determine if the net force on an ion is inward, outward, or equilibrium?
2 possible ways: -calc net driving force for the ion (Vm-Ei) Ei = -(61/z)log(in/out) -calc electrochemical potential of ion ∆μ = 61log(in/out) + zVm
if DF or ∆μ is negative, cats in ans out if DF or ∆μ is positive, cats out ans in if DF or ∆μ is 0, no net movement *DF and ∆μ always have same sign... ...they differ by factor of z
at 20 degrees C, equilibrium potential of an ion =
Ei = -58/z log(in/out)
at 37 degrees C, equilibrium potential of an ion =
Ei = -61/z log(in/out)
in physiological temperature, equilibrium potential of an ion =
Ei = -61/z log(in/out)
at (British) room temperature, equilibrium potential of an ion =
Ei = -58/z log(in/out)
how is the VGNa+ channel a-gate opened?
depolarization (+ charges on inner membrane) force + residues of the a-gate (on the inner side of the gate) apart
is the VGNa+ channel a-gate nearer the internal or external side of the membrane?
internal
when does the VGNa+ channel i-gate bind the channel?
after a delay, the i-gate binds the open a-gate
when does the VGNa+ channel i-gate release the channel?
only after repolarization closes the a-gate
how does the VGNa+ channel i-gate interact with the a-gate?
binds a-gate when open
releases a-gate when closed
how is the peak of an AP affected when external [Na+] is reduced? why?
peak decreases
because Ena = -61/z log(in/out) is decreased,
so DF = Vm-Ena is decreased,
and less driving force drives less Na+ through VGNa+ channels
how is the peak of an AP affected when internal [Na+] is increased?
peak decreases
because Ena = -61/z log(in/out) is decreased,
so DF = Vm-Ena is decreased
and less driving force drives less Na+ through VGNa+ channels
when extracellular Na+ is decreased, how does this affect AP shape?
- slower rate of depolarization
- lower peak
- same repolarization rate
- same undershoot
when extracellular Na+ is decreased, how does this affect AP repolarization and undershoot?
it doesn’t
these depend on VGK+ channels
how does increased extracellular K+ affect AP shape?
- same depolarization rate
- slightly higher peak
- slower repolarization rate
- less undershoot
why doesn’t V resting change when we experimentally alter K+ or Na+ concentrations on either side of the cell membrane?
because we alter Cl- concentrations as well – to maintain macroscopic electroneutrality (otherwise Vm changes would be wild)
how does decreased extracellular K+ affect AP shape?
- same depolarization rate
- slightly lower peak
- faster repolarization rate
- deeper undershoot
how does TEA affect action potential shape?
TEA blocks K+ channels
- same depolarization rate
- slightly higher peak
- very slow repolarization rate (leak channels)
- no undershoot
when stimulated with maximum frequency, how is the afterpotential for an axon with glial cells different from that of the same neuron without glial cells?
glial cells surround axon and keep ejected K+ from diffusing away, so:
- so with glial cells, ECF [K+] gets progressively higher with each AP, so Ek and Vm increase slightly and afterpotential increases
- without glial cels, K+ diffuses away into ECF and cell is easier to repolarize back to normal afterpotential
on which ion does afterpotential depend?
K+
what accounts for the post-tetanic extra-hyperpolarization of a small axon?
post-tetanic increased ECF K+ concentration and increased ICF Na+ concentration stimulates the Na-K-ATPase pump to higher activity, which hyperpolarizes the membrane extra
why are post-tetanic extra-hyperpolarizations not seen as commonly in large axons?
because the post-tetanic extra-hyperpolarization effect depends on high ECF K+ concentration and high ICF Na+ concentration that stimulate KK-NaNaNa pump to higher activity and hyperpolarizes the membrane extra
-in a large fiber, the K+ and Na+ concentration changes are not as significant due to smaller surface area / volume ratio.
what does oubain do to membrane transport?
inhibits Na-K-ATPase pump
how does oubain affect post-tetanic extra-hyperpolarization?
limits it because oubain inhibits Na-K-ATPase pumps
(post-tetanic increased ECF K+ concentration and increased ICF Na+ concentration stimulates the Na-K-ATPase pump to higher activity, which hyperpolarizes the membrane extra)
