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Flashcards in Action Potential Deck (62):

What is the time constant?

The amount of time it takes for the voltage to change by a certain percentage (63%) of the eventual new steady state value



What is the length constant?

The distance between the injection site and the point where the steady state transmembrane voltage change has decayed by 63% from its peak value.


What happens to the size of the action potential as it goes down an axon?

Stay the same


What is the "all or nothing" principle?

Size of action potential does not depend on the size of the triggering stimulus


What are the six stages of a membrane depolarization, starting with the cell at rest?

1. Cell at rest; polarized-cell negative inside
2. Depolarization phase - sometimes called rising phase
3. Overshoot - variable
4. Peak of action potential
5. Repolarization phase - sometimes called falling phase
6. Hyperpolarization; sometimes called undershoot phase


What is the ionic basis for the depolarization phase?

Opening if Na channels, causing Na to rush in


What is the ionic basis for the repolarization phase?

Na channels close (inactivation gate)
K channels open to allow K to rush outside the cell


What is the ionic basis for the hyperpolarization phase?

K channels remain open long enough to go past the resting membrane potential


If Na/K pumps are disable, say through oubain poisoning, how long are nerve fibers still competent?

Many thousands of nerve impulses


What are the two domains of the Na/K pump?

Activation gate and inactivation gate


When the Na channel is in its resting state, what is the state of the activation gate? Inactivation gate?

Activation gate= Closed
Inactivation gate = open


What causes the activation gate to swing open?

Rise in membrane potential


What is the inactivation state of the Na/K pump?

When the inactivation gate is closed


What closes the inactivation gate?

Same change in membrane potential as the activation gate, but it closes more slowly.


True or false: The Na+ channel cannot go directly from the inactivated to the activated state; it must first go back to the resting state.



What causes the change in the Na/K pump from the inactivation state to the resting state?

Change in membrane potential back to the resting potential


What activates the K channels (opens them)?

Depolarization, but takes longer to open


What are the K channels responsible for?

The re-polarization of the membrane


What is the meaning of a threshold (what chemically determines this)?

The value of membrane potential at which inward flow of Na+ exceeds the passive outward flow of K


Where is the threshold of an axon usually the lowest?

At the initial segment of the axon


Where is the "initial" segment of the axon?

Axon hillock to about 20-50 μm down the axon


What happens in hypocalcemia?

The probability that a Na channel will open is greatly increased (hyper sensitivity of nerves)


What is the clinical consequence of hypocalcemia and hypoparathyroidism?

Hypoparathyroidism leads to reduction in serum calcium levels and a tendency for muscles to begin twitching spontaneously.


What are the three types of electrical signals that occur in the body?

1. Receptor signals
2. Synaptic potentials
3. Action potentials


The cell membrane can be modeled as a simple circuit. Which part of the membrane is a capacitor, and which part is a resistor?

Capacitor = bilayer
Resistor = ion channels


What happens to the permeability of Na/K as it goes from the resting state, to the depolarized state, to the repolarized state?

Resting, K>>Na
Depolarizaed: K<>Na


How do local anesthetics work?

Block Na channels through various routes


What determines the voltage threshold of an action potential?

The minimal voltage needed to kick the Na channels into the fast positive feedback cycle


What are the three factors that determine the AP threshold?

Na channel
K channel


What happens in hypocalcemia to neurons?

Hyper sensitivity d/t lowering of threshold


What are the four clinical manefistations of hypocalcemia?

1. Convulsion
2. Arrhythmias
3. Tetany
4. Spasms and stridor



What is chvostek's sign?

Contraction of the muscles of the eye, mouth, or nose elicited by tapping over the facial nerve in front of the ear. Seen sometimes in hypocalcemia


What is trousseau's sign?

Muscles spasms that results after application of a BP cuff that is raised to higher than SBP


What is the physiological effect of hypercalcemia on the action potential threshold?

Raises it (the probability that a Na+ channels is open at a certain voltage is decreased )


What are the clinical manifestations of hypercalcemia?

Decrease in neuromuscular irritability


What is a condition that results in hypercalcemia?



Does [Ca] change the resting potential of a membrane? Why or why not?

No, the cell membrane is not permeable to it


How does Ca change the threshold potential?

Changing the Na channel opening probability


At low [Ca] is it easier or more difficult to open Na channels?



How does extracellular [Na] affect the rise time and shape of an action potential?

Lowering the extracellular [Na] reduces both the rate and rise of the action potential, and its peak amplitude


What accounts for the plateau seen in cardiac muscle cell action potential?



What is the refractory period?

Period of time after the absolute refractory period during which you'd need a stronger than normal stimulus to elicit a new action potential


What is the absolute refractory period? How long is it usually?

The period of time when an action potential cannot be generated regardless of conditions

Usually just the duration of the actual action potential


What is the chemical basis for the absolute refractory period?

The Na channels are stuck in an inactivated state


What is the chemical basis for the relative refractory period?

The delayed K channel opening and hyperpolarization

K+ ions leaving the cell oppose the depolarizing effect of opening Na+ channels


What sets the upper limit of firing frequency?

The relative refractory period


What creates the phenomenon of propagation?

When one patch of a neuron is depolarized, it creates a current of ion flow in/out in neighboring patches, which do likewise (but at a lesser degree)


What will happen if an action potential is set up in the middle of a neuron?

The action potential will flow in both directions


What ensure that an action potential only flows in one direction?

The axon hillock's lower action potential threshold


How does the axon diameter affect the conduction velocity? How?

Larger = faster

Since the electrical resistance decreases faster than the capacitance increases, increasing axon diameter increases the speed of conduction.


When the diameter of an axon increases, what happens to its resistance?

decreases in proportion to the square of the radius of the axon (area of the axon)


When the diameter of an axon increases, what happens to its capacitance?

Increases in direct proportion to the radius of the axon (C = 2πr)


How does the mylenation of axons contribute to the velocity of the action potential?

Greatly decreases the axon membrane capacitance, and increases the membrane resistance


What is mylein composed of?

Lipids, cholesterol, other non-conducting proteins


What is the myelinating cells in the PNS?

Schwann cells


What is the myelinating cells in the CNS?



What is the effect of schwann cells?

Allows nerves to only form circuits at the nodes of ranvier, since these are the only places that Na channels are


Where can action potentials be generated in a myelinated nerve?

Only at the nodes of ranvier


Why is conduction speed increased with myleination (chemially)?

Capacitance is lower, and do not waste time generating small action potentials everywhere


Is myleinating nerves energy efficient or inefficient? Why?

Efficient, because there are fewer spots that have action potentials generated, meaning fewer Na/K pumps


What is the cause of MS?

Antibodies attacking oligodendrocytes, causing demyelination of the CNS


What is Guillain-Barre Syndrome, and what is is caused by?

Antibodies mistakenly attack the PNS Schwann cells, causing demyelination. This is usually reversible.