What we think, what we feel, what we do… all of this depends to a great extent on our Nervous System, thanks to which we can manage each of the processes that occur in our body and receive, process and work with the information that this and the environment provide us.

The operation of this system is based on the transmission of bioelectric pulses through the different neuronal networks that we have. This transmission involves a series of very important processes, one of the main ones being the so-called action potential .

Action potential: basic definition and characteristics

The action potential is understood to be the wave or electrical discharge that arises from the set to the set of changes that the neuronal membrane undergoes due to electrical variations and the relationship between the external and internal environment of the neuron.

This is a single electrical wave that will be transmitted through the cell membrane until it reaches the end of the axon , causing the emission of neurotransmitters or ions to the membrane of the post-synaptic neuron, generating another potential for action that will eventually bring some kind of order or information to some area of the body. It begins in the axonic cone, near the soma, where a large number of sodium channels can be observed.

The potential for action has the particularity of following the so-called law of all or nothing. That is to say, either it is produced or it is not produced, there being no intermediate possibilities. Despite this, whether or not the potential appears can be influenced by the existence of excitatory or inhibitory potentials that facilitate or hinder it.

All the action potentials will have the same charge, but the only difference is the amount: a message that is more or less intense (for example, the perception of pain from a puncture or stabbing will be different) will not generate changes in the intensity of the signal, but will only cause action potentials to be realized more frequently.

In addition to this and in relation to the above, it is also worth commenting on the fact that it is not possible to add action potentials, since have a short refractory period in which that part of the neuron cannot initiate another potential.

Finally, the fact that the action potential is produced in a specific point of the neuron and has to be produced along each of the points of the neuron that follow it, not being able to turn the electrical signal back.

Phases of action potential

The action potential is produced along a series of phases, which go from the initial resting situation to the sending of the electrical signal and finally the return to the initial state.

1. Resting potential

This first step implies a baseline state in which no alterations have yet taken place leading to the potential for action. This is a moment when the membrane is at -70mV, its base electrical charge . During this moment some small depolarisations and electrical variations can reach the membrane, but they are not sufficient to trigger the action potential.

2. Depolarization

This second phase (or first phase of the potential itself), the stimulation generates an electrical change in the membrane of the neuron of sufficient excitatory intensity (which should at least generate a change up to -65mV and in some neurons up to -40mV) to generate that the sodium channels of the axon cone open, so that the sodium ions (positively charged) enter in a massive way.

In turn, the sodium/potassium pumps (which normally keep the inside of the cell stable by exchanging three sodium ions for two potassium ions so that more positive ions are expelled than enter) stop working. This will cause a change in the charge of the membrane, so that it reaches 30mV. This change is known as depolarization.

After that the potassium channels of the membrane start to open, which being also a positive ion and being entering these massively will be repelled and start to leave the cell. This will cause the depolarization to be slowed down, as positive ions are lost. That is why at most the electrical charge will be 40 mV. The sodium channels will be closed, and will be inactivated for a short period of time (which prevents summative depolarization). A wave has been generated that cannot be reversed.

3. Repolarization

As the sodium channels have closed, sodium can no longer enter the neuron , while the fact that the potassium channels remain open means that it continues to be expelled. This is why the potential and the membrane become increasingly negative.

4. Hyperpolarization

As more and more potassium is released, the electrical charge of the membrane becomes increasingly negative to the point of hyper-polarisation : it reaches a level of negative charge that even exceeds that of rest. At this point, the potassium channels close, and the sodium channels are activated again (without opening). This means that the electrical charge stops dropping and that technically there could be a new potential, but the fact that it suffers from hyperpolarisation means that the amount of charge that would be necessary for an action potential is much greater than usual. The sodium/potassium pump is also reactivated.

5. Resting potential

The reactivation of the sodium/potassium pump generates that little by little a positive charge enters inside the cell, something that finally will generate that it returns to its basal state, the rest potential (-70mV).

6. The action potential and release of neurotransmitters

This complex bioelectric process will be produced from the axon cone to the end of the axon, so that the electrical signal will be advanced to the terminal buttons. These buttons have calcium channels that open when the potential reaches them, something that causes the vesicles containing neurotransmitters to emit their contents and expel them into the synaptic space. Thus, it is the action potential that generates the release of the neurotransmitters, being the main source of transmission of the nervous information in our organism.

Bibliographic references

  • Gómez, M.; Espejo-Saavedra, J.M.; Taravillo, B. (2012). Psychobiology. Manual CEDE de Preparación PIR, 12. CEDE: Madrid
  • Guyton, C.A. & Hall, J.E. (2012) Treatise on Medical Physiology. 12th edition. McGraw Hill.
  • Kandel, E.R.; Schwartz, J.H. & Jessell, T.M. (2001). Principles of neuroscience. Fourth edition. McGraw-Hill Interamerican. Madrid.