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Discuss the generation and propagation of action potentials.

In which ion gradient is the potential energy for formation of an action potential stored? How is this energy used to generate an action potential? How is an action potential initiated? What is meant by all-or-nothing response?

Graphically illustrate how axonal membrane potential changes with passage of an action potential. At various times in an action potential, describe the following: membrane voltage, sensitivity of sodium channel to voltage, sodium channel conductance, sensitivity of potassium channels to voltage, and potassium channel conductance.

Explain how the activity of a voltage-gated sodium channel depends on its structure.

How are action potentials propagated in unmyelinated and myelinated axons?

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Jean Keeling
Jean KeelingLv2
11 Jan 2019
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Related questions

Please help

29. The action potential


a. begins with the membrane’s increased permeability to potassium.

b. returns to resting when the sodium channels open.


c. can be triggered by opening of ligand gated Na and K channels.


d. involves voltage-gated Chloride channels in the membrane.


e. can be triggered by opening of voltage gated Na+ and K+ channels.

30. Which of the following is not a step in the propagation of action potentials?


a. Sufficient local inward current causes the axon to reach threshold.


b. Local depolarization/inward current spreads to adjacent axonal regions.


c. Adjacent regions eventually reach threshold and exhibit an action potential waveform.


d. Current/depolarization continue to spread directionally along the axon, repeating steps a–c

e. All of the above are steps contributing to the propagation of action potentials.

31. Which of the following is important for the unidirectional propagation of action potentials?

a. The voltage dependence of the sodium channels


b. The voltage dependence of the potassium channels


c. The presence of a refractory period at a location where an action potential has just fired

d. Sufficient “leakiness” of the axons, such that backward propagation of action potentials is prevented


e. The capacity of axons to function as perfect insulators and prevent current leakage and backpropagation

Santiago Ramon y Cajal’s theory of dynamic polarization refers to the:

(a)membrane potential of a neuron at rest.

(b)membrane potential of a neuron firing action potentials.

(c)opening and closing of gated channels in the membrane.

(d)one way flow of information in neurons from dendrites to axon terminals.

(e)one way flow of information in neurons from axon terminals to dendrites.

Over the course of scientific history, there are many examples of scientists reaching the right conclusion for the wrong reasons. When Schwann first proposed that the nervous system was made of individual cells, he based it on observations of:

(a)synapses.

(b)dendrites

(c)axon terminals.

(d)astrocytes.

(e)Nodes of Ranvier.

The synaptic cleft was finally seen in the 1950s. What prevented scientists from seeing it earlier?

(a)The resolution of the light microscope.

(b)They were looking in the wrong place.

(c)Their tissue was not appropriately stained.

(d)Myelination of the axons.

(e)all of the above

The resting membrane potential of a neuron is approximately:

(a) +65 V

(b) +65 mV

(c) -65 V

(d) -65 mV

What is largely responsible for the resting membrane potential in a neuron?

(a)Axonal insulation by myelin

(b)Voltage-Gated Sodium Channels

(c)The Action Potential

(d)Potassium Leak Channels

Which of the following would DECREASE the propagation velocity of an action potential down an axon?

(a)Increase in axon diameter

(b)Increase myelination between nodes of Ranvier

(c)Remove myelination between nodes of Ranvier

(d)Decrease density of voltage-gated Na+ channels except at the Nodes of Ranvier

The resting membrane potential of a neuron can be estimated using the:

(a)Nernst equation

(b)Goldman equation

(c)Hodgkin and Huxley equation

(d)Ohm’s law

18. What would happen to the resting membrane potential of a neuron if you added K+ to the extracellular fluid?

(a)Resting membrane potential would increase (become more positive)

(b)Resting membrane potential would decrease (become more negative)

(c)Resting membrane potential would not change

(d)Resting membrane potential would be abolished

. Which of the following statements is FALSE for Graded Potentials

(a)Magnitude changes with magnitude of triggering stimulus

(b)Magnitude decreases with distance from initial site

(c)Cannot be summed

(d)No refractory period

In the nervous system, the strength of the stimulus is coded into:

(a)The frequency of action potentials generated

(b)The amplitude of action potentials generated

(c)Both the frequency and amplitude of action potentials generated

(d)The duration of individual action potentials generated

Ion movement during both the depolarization and repolarization phases of an action potential are the result of:

(a)active transport pumps along the neuron membrane.

(b)diffusion of ions down their electrochemical concentration gradients.

(c)negative feedback loops.

(d)All of the above

At the peak of the action potential, the membrane potential is:

(a)Exactly at the Na+ equilibrium potential

(b)Greater (more positive) than the Na+ equilibrium potential

(c)Above 0 mV but less positive than the Na+ equilibrium potential

(d)0 mV

How does spacing apart sodium and potassium channels allow theaction potential to travel faster down the axon? This is the reasonalways cited for saltatory conduction and myelination, but mymental model of conduction tells me that the density of ion gatesalong the axon should not affect the speed of the AP.

To illustrate, consider a myelinated axon. A wave of Na+ fromaction potential site 1, a node of Ranvier, rushes into and quicklydiffuses down the axon. (It travels in both directions, butbackwards is still in the refractory period.) It diffuses throughthe myelinated region, its concentration always diminishing. Beforeit attenuates too much, however, it happens upon node of Ranvier 2,where it triggers another action potential. A new wave of Na+rushes in and the cycle repeats. This should be plain so far.

Now imagine that there is actually a node of Ranvier halfwaybetween node 1 and 2, called node 1.5. The wave of Na+, on its wayto node 2, happens to trigger an action potential at node 1.5, fromwhich a wave of Na+ pours in and either boosts the original wave orreplaces it by taking its momentum. Now the reinforced waveproceeds to node 2 and triggers it just as soon as, perhaps evensooner than, if node 1.5 had not existed. Repeatedly insert nodesat higher densities until the situation is simply lack ofmyelination, and we conclude that unmyelinated axons can transmitan action-potential-triggering wave of Na+ as fast as or fasterthan a myelinated one.

In short, my point of confusion is this: I cannot seehow a higher density of gated channels can possibly slow down thewavefront of Na+ that triggers action potentials. Ifanything, the additional influxes of Na+ should speed up theall-important wavefront, assuming that new waves really "eitherboost the original wave or replace it by taking its momentum", andalso assuming that the wavefront of Na+ is really all-important forsignal transmission, and also assuming that the mere presence of(voltage?) gated ion channels in the membrane does notsignificantly retard the wavefront.

But the usual explanation for why saltatory conduction is fasterthan continuous conduction (a fact I hope is empirically andunambiguously established) relies on the putativeslowing effect of ion channels on the signal fore. Please explainthis effect in more detail, if it is not amisconception.

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