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To my understanding, the steps of an action potential are as follows:

  1. The neuron is at rest--there is a negative charge (K ions) inside the cell, and a positive charge (Na ions) outside the cell. Pumps work hard, pumping in K and pumping out Na to maintain this polarization.

  2. Excitatory NTs bind with the dendrites. As soon as it's over a certain threshold it triggers an action potential.

  3. The inside of the cell depolarizes, and the depolarized "chunk" propagates through the axon.

Now here's my confusion:

A. How do neurotransmitters manage to depolarize the inside of the cell? Do they force the cell to give up pumping out Na ions? Do the neurotransmitters themselves contain positively charged ions that the ion pumps are not sensitive to?

B. When the cell depolarizes, the electrical impulse travels down the axon. When this happens, Na+ and K+ ions rapidly pass through the membrane as the signal fires. (Like this picture) http://en.wikipedia.org/wiki/Action_potential#mediaviewer/File:Action_Potential.gif

Why are ions being pumped in and out of the axon in such a way to propagate an action potential? Why isn't it just a positively charged signal running through the axon, without regard to the outside environment? (please let me know if this is unclear!)

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I will try to answer all of your main and sub questions structurally below:

How do neurotransmitters manage to depolarize the inside of the cell?

  1. Do they force the cell to give up pumping out Na ions?
    No, the Na,K-ATPase (the sodium potassium pump) keeps active, also during the action potential (AP).
  2. Do the neurotransmitters themselves contain positively charged ions that the ion pumps are not sensitive to?
    They can, but neurotransmitter charge is irrelevant.
  3. Answer: Neurotransmitters bind to their corresponding receptors. An example excitatory neurotransmitter is glutamate (Glu). Glu has many receptors and one of them is the NMDA receptor. The NMDA receptor is coupled to a cation channel that opens when Glu binds (and other conditions pertain). In turn Na+ and other depolarizing cations can enter the cell through the open channel. Other neurotransmitters and receptor mechanisms exist, but the coupling to a cation channel is a commonly encountered theme.


When the cell depolarizes, the electrical impulse travels down the axon. When this happens, Na+ and K+ ions rapidly pass through the membrane as the signal fires. [...]

  1. Why are ions being pumped in and out of the axon in such a way to propagate an action potential?
    During an action potential, the voltage changes are not the result of ions being pumped in or out of the cell. Instead, ions flow along their concentration and charge gradients out or in the cell during an action potential. For example, Na+, a key ion in any action potential, flows passively into the cell during an action potential. Passive influx occurs, because Na+ is continuously and actively pumped out of the cell into the extracellular fluid by the Na,K-ATPase. Moreover, the inside of the cell is highly negatively charged. Both the concentration gradient and charge gradient (i.e., the potential difference) will cause Na+ to surge into the cell once Na+ channels open. How then does it move across the axon? The trick is that Na+ depolarizes the cell membrane. When for example Glu binds to its NMDA receptor, Na+ enters the cell into the dendrite. Then, voltage-gated ion channels take over. Voltage-gated ion channels open or close depending on the local membrane potential. Most notably, voltage-gated sodium channels (VGSCs) open when the cell membrane depolarizes. Hence, after NMDA receptors are activated in the dendrite, Na+ enters. This in turn depolarizes the dendrite and VGSCs open. This causes further depolarization and adjacent VGSCs open etc. etc. Voltage-gated potassium channels open after the VGSCs and re-polarize the membrane. An overview is provided in the following image from Antranik.org :

action potential

  1. Why isn't it just a positively charged signal running through the axon, without regard to the outside environment?
    Charges only move to an opposite charge. A neuron is not differentially charged from dendrite to axon terminal. Hence another way of action potential transduction is needed. Step-wise opening of VGSCs is a clever trick to use a constant cell membrane potential to generate a directional action potential.
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  • $\begingroup$ Not sure how best to suggest a change to answer #5, but the main issue I have is that, directly contrary to the OP's point, there is a passive flow of voltage down the length of the axon (in both directions); directly adjacent VGSCs are not necessary for this, and often are not even present (until the next node of Ranvier). The presence of the voltage gated channels is to increase the length that the AP will travel, not make it travel at all. And the directionality is not directly due merely to the presence of the channels, but the fact that they inactivate. $\endgroup$ – Chelonian Jul 12 '15 at 17:45
  • $\begingroup$ @Chelonian - thanks for your 'cation' edits! This comment, however, I don't agree with. First, voltage doesn't flow. Second, VGCs are crucial for APs. Third, not all axons are myelinated. Fourth, even in myelinated ones it is the the positioning of VGC patches that guide the AP. It's just saltatory from node to node. Fifth, the VGCs are indeed there as amplifiers, but without them there would be no AP. Sixth, directionality is for sure governed by serial opening of VGCs! It is Unidirectionality that is maintained by inactivation. Last, the question is too broad for fine detailed answers. $\endgroup$ – AliceD Jul 12 '15 at 23:46
  • $\begingroup$ 1) Right; should say passive spread of charge resulting in a change in voltage down axon. 2) Never said VGCs weren't crucial for APs, 3) or that all axons were myelinated, just that (in myelinated ones) Na+ channels aren't present until nodes. 4) Don't understand this but I can't imagine we disagree. 5) Of course. So? 6) What's the difference between "directionality" and "unidirectionality"? I mean simply that APs only head distally because the VGC soma-ward are inactivated; if they weren't, APs would go both directions. 6) Your answer strikes me as incorrect, not lacking in details. $\endgroup$ – Chelonian Jul 13 '15 at 19:10
  • $\begingroup$ @Chelonian, perhaps we should take this to chat. Also, if you think you have a better answer, you could put it into an answer? $\endgroup$ – AliceD Jul 13 '15 at 20:45
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To answer your question #5:

"Why are ions being pumped in and out of the axon in such a way to propagate an action potential?

As AliceD's answer provided, the ions during an action potential are not being pumped, and don't even need to be pumped, but just passively flow into or out of the axon due to the forces of electricity and diffusion. As an example, imagine a water balloon filled with dye, and you prick it with a pin underwater: the balloon need not pump the dye out, it will just diffuse out.

Why isn't it just a positively charged signal running through the axon,

There is a passive spread of charge down the length of the axon, at least for some short distance. However, axons are generally too long for that spread to get all the way to the end of the axon. Therefore, the signal must be amplified over and over down the length of the axon in order to (attempt to) insure it gets to the end.

without regard to the outside environment?"

Just a point of language here: When speaking of voltage (AKA potential), you need to refer to two positions, and when discussing the action potential we use the inside of the axon relative to the outside.

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