Action Potentials Flashcards
What determines the threshold voltage?
It’s the point at which sodium and potassium currents are exactly equal and opposite
If threshold is surpassed; what happens with regard to Na+?
A positive feedback loop with sodium ions entering the cell and opening more sodium channels. Soon; all sodium channels are open and Vm is on its way to Ena.
What 2 general events happen to cause repolarization?
1: PNa declines back to its resting level 2: PK undergoes a transient increase
How does the level of PNa decrease (think fast and slow sodium gates)?
There are 2 gates in the sodium channel: the activation gate (m) is closed during rest and opens quickly to cause depolarization. The inactivation gate (h) is open at rest and closes upon deploarization. The inactivation gate closes more slowly; so there is a period of time when the channel is open for Na+ to come in. Once the inactivation gate closes; the level of PNa decreases.
What is happening with K+ during rest/depolarization/repolarization?
A negative feedback loop. Kv channels are closed at rest. Depolarization causes them to open; which causes repolarization; which causes them to shut
Why are potassium channels important for action potential?
They allow for FASTER repolarization. Note: without them the cell would repolarize with the closure of Na+ inactivation gates and passive (ungated) K+ channels; just more slowly
What physically is the main cause of the refractory period?
Results primarily from the fact that the sodium channel inactivation (h) gates require time to reopen after repolarization. If stimulus is applied when some h gates are still closed; the sodium channel activation (m) gates may swing open but no Na+ can flow owing to the closed inactivation gates.
How do the K+ channels contribute to the refractory period?
After repolarization; it takes several msec for the K+ channel gates to close again. The higher K+ conductance makes it harder for a stimulus to depolarize the axon.
Why doesn’t slow depolarization cause an action potential (AKA accommodation)?
Slow depolarization provides time for the inactivation gates to close first; so when activation gates do open any channel in which the inactivation gate has already closed cannot conduct sodium ions
How does accommodation manifest during hyperkalemia?
Elevated plasma potassium ion concentration causes steady membrane depolarization and closes some inactivation gates. When a physiological stimulus arrives to produce a rapid depolarization; inactivated cannot contribute to the action potential. This is the mechanism that underlies the generation of cardiac arrhythmias
Do bigger or smaller axons need to use their Na/K pumps more freqently?
Small axons (they have a higher surface area to volume ratio).
How does local anesthetic work?
Blocks sodium channels - keeps activation gates from opening. Axon cannot propogate the action potential
What is the safety factor?
The density of Na channels must be enough to supply enough current to depolarize the next bit of membrane. The safety factor of transmission is 5-10 times the minimum required for successful propagation
What is the advantage of the safety factor of transmission (why have excess Na channels)?
1: when axons branch the membrane just before the branch must deliver sufficient current to depolarize both branches. 2: the absolute refractory period will end sooner if there is an excess of Na channels in the membrane (RP ends when enough inactivation gates have reopened to enable the axon to conduct again).
When an axon is stimulated how many APs are generated?
- One traveling in each direction
