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
The rate of the Na-K pump is proportional to
accumulation of Na+ inside and accumulation of K+ outside
Glial cells are exclusively permeable to __, so their resting transmembrane potential (Em) is
K+
Thus, their Em=Ek= -90mV
Note how the Em of glial cells closely follows the nernst potential line of K+
How do glial cells help regulate the extracellular environment of neurons?
When neurons are extremely active, extracellular K+ may build up in the interstitial fluid faster than pumps can put them back in the neuron –> Glial cells take up excess K+
Spatial buffering & siphoning
Spatial buffering steps
- The rise in [K+]out during increased neuronal activity depolarizes glial cells locally by altering the value of K+’s nernst potential
- Depolarization spreads passively to neighboring glial cells via gap junctions
- K+ ions enter the glial cells and carry current away from this region via gap junctions
Thus K+ ions are diffuse deposited into the extracellular fluid of remote regions where the neurons are less active
Siphoning
K+ ions are taken up in various regions of the glial cell membrane and dispersed at another region of the membrane with a high density of K+ in the endfeet of the glial cells that contact the vitreous humor of the eye.
These excess K+ ions are siphoned into the vitreous humor, removing it from retinal cells
Asatrocytes may release K+ into the bloodstream to remove excess K+ in the vicinity of neurons
A patient is given a drug that produces an adverse reacion, causing neuronal membrane permeability to increase to all ions. Which of the following changes in resting membrane potentials, or action potentials would most likely occur?
- Resting membrane potential would approach EK
- Resting membrane potential would not change much
- Resting membrane potential would approach zero mV
- Action potential would increase in amplitude
- Steady-state inactivation would decrease
Resting membrane potential would approach 0 mV
Hypocalcemia- lowering serum calcium. How will this affect patient’s excitable cells?
- Excitabilitly will increase
- AP threshold will increase
- Na+ channel activation will decrease
- K+ channel activation will decrease
Excitability will increase
At central synapses, repetitive activity can cause short-term facilitation of EPSP amplitude,s followed by depression of EPSP amplitudes as repetitive firing continues. The depression phase is most likely caused by which of the following mechanisms?
- Upregulation of the transporter for the re-uptake of the excitatory transmitter
- Upregulation of the enzyme for hydrolysis of the excitatory transmitter
- Accumulation of Ca2+ in the nerve terminal
- Depletion of Ca2+ in the nreve terminal
- Depletion of filled vesicles in the nerve terminal
Depletion of filled vesicles in the nerve terminal
A dehydrated marathon runner is having muscle twitches and has a serum sodium of 158meq/L (hypernatremic). What effect do we expect to see in his patient’s resting membrane potential and AP amplitude?
Little change in RMP
Increased AP amplitude
A patient is given a drug that increases steady state inactivation of voltage-gated Na channels. What impact will this have on RMP, AP amplitude, and AP threshold?
RMP- No change
AP amplitude- decreased
AP threshold - increased
