Neural Control and Coordination · Lesson 4 of 8
Action Potentials and Propagation Along Axons
“Threshold, voltage-gated Na⁺ and K⁺ channels, depolarisation, repolarisation, refractory periods and saltatory conduction.”
• Trace the stages of an action potential from threshold to recovery. • Identify how Na⁺ influx and K⁺ efflux change membrane voltage. • Explain local currents and propagation from one axonal region to the next. • Compare continuous propagation with saltatory conduction at nodes. • Distinguish action-potential amplitude from impulse frequency and direction.
How can a signal travel along a living cell?
A neuron receives numerous small electrical inputs. If their combined effects raise the membrane potential at an excitable region to threshold, voltage-gated Na⁺ channels open rapidly. Na⁺ moves into the cell down its electrochemical gradient, making the inside less negative and temporarily positive relative to the outside. This regenerative local electrical event is the beginning of an action potential. Nearby membrane then responds, so the electrical event travels along the axon without needing an individual Na⁺ ion to run from one end to the other.
A rapid, regenerative and stereotyped change in membrane voltage produced by coordinated opening and inactivation of voltage-gated channels.
A change in membrane potential toward a less negative or more positive interior.
A return of membrane voltage toward its resting negative level after depolarisation.
Threshold and all-or-none response
An action potential is triggered only when a sufficient local change in voltage activates enough voltage-gated Na⁺ channels to generate a positive feedback loop: depolarisation opens more channels, which permits more Na⁺ influx, which causes further depolarisation. Below threshold, a small input may decay without becoming a propagating action potential. Above threshold, the action potential generally reaches a characteristic amplitude, subject to the type and state of neuron.
The 'all-or-none' principle applies to action potentials in an individual axon, not to whether an entire muscle or body must respond maximally. Stronger stimuli can increase the number or frequency of action potentials and recruit additional neurons; they do not simply make one normal action potential twice as tall.
Stage one: rapid Na⁺ entry
When threshold is reached, activation gates of voltage-gated Na⁺ channels open quickly. Because the Na⁺ concentration is higher outside and the interior is initially negative, Na⁺ flows inward. The inside potential rises toward positive values, sometimes reaching roughly +30 mV in a typical illustrative neuron. The source describes this as reversal of polarity at an excited site: the inner surface becomes locally positive relative to the outer reference.
This Na⁺-dependent event does not require the sodium–potassium pump to reverse. Instead, Na⁺ crosses through specialised channels following the electrochemical gradient already established in the resting state. The voltage change is rapid because channel opening is regenerative.
Stage two: Na⁺ channel inactivation and K⁺-driven repolarisation
Within a short interval, most of the voltage-gated Na⁺ channels enter an inactivated state, reducing further Na⁺ entry. Delayed voltage-gated K⁺ channels are open, permitting K⁺ to flow outward. Loss of positive charge shifts membrane voltage back toward negative values. This is repolarisation. K⁺ channels may remain open after the voltage has reached its usual resting level, causing a brief after-hyperpolarisation in which the inside is temporarily more negative than usual.
The membrane then returns toward resting channel states. The Na⁺/K⁺ pump maintains concentration gradients over repeated activity, but K⁺-channel-mediated outward current is the main rapid repolarising force in this simple model. A good explanation should therefore not claim that the pump alone instantly pushes out all the Na⁺ that entered during each impulse.
A voltage–time curve makes the phases visible
Why an impulse spreads from point A to point B
The source describes a region A of axon membrane that becomes depolarised while an adjacent region B is still at rest. Because the membrane voltage differs along the axon, a local circuit of electrical current flows. Inside the axon, positive current spreads from the depolarised region toward a more negative neighbouring region. Outside, return current completes the circuit. The resulting depolarisation of region B brings its voltage-gated Na⁺ channels toward threshold.
Once B reaches threshold, it generates a fresh action potential. The active event at B creates local currents into the next region, so the wave propagates. The actual signalling occurs through sequential regeneration, not through one pulse of charged liquid being physically pushed down an intact axon. This is why the impulse can travel long distances without continuously decreasing in amplitude under normal conditions.
Why an action potential normally travels forward
A time after an action potential during which the membrane is unable or less able to initiate another full action potential.
Immediately after firing, many Na⁺ channels are inactivated and cannot reopen until the membrane repolarises sufficiently. During this absolute refractory period, a second normal action potential cannot be generated in that region. As channels recover and some K⁺ conductance remains elevated, the membrane enters a relative refractory period requiring stronger stimulation. These recovery processes help prevent the recently activated region from being excited again by its own local current.
Under ordinary conditions an axon action potential initiated at its initial segment propagates toward terminals because the region behind the wave is refractory. However, an artificially stimulated point in the middle of an axon may conduct in both directions, demonstrating that the basic membrane machinery is not inherently a one-way diode; direction also depends on where the impulse originates and which regions are refractory.
Unmyelinated propagation: continuous regeneration
In an unmyelinated axon, voltage-gated channels distributed along the membrane support action-potential generation at successive neighbouring regions. Each region must charge its membrane and open channels, so propagation is usually slower than in a similarly sized myelinated fibre. Diameter still matters: a larger diameter reduces internal resistance and can increase conduction speed even when myelin is absent.
Myelinated propagation: saltatory conduction
Rapid apparent jumping of an action potential between nodes of Ranvier along a myelinated axon, with fast passive current spread beneath myelin.
Myelin increases membrane resistance and reduces capacitance across internodal segments. Current can spread across these insulated regions while the action potential is regenerated at exposed nodes rich in voltage-gated Na⁺ channels. Rather than an impulse needing full regeneration at every tiny stretch, it appears to jump from node to node. This is saltatory conduction and normally increases speed and reduces some energy costs of restoring ionic gradients.
The signal does not teleport. Electrical current spreads continuously inside the axon, and membrane excitability is concentrated at the nodes. The 'jumps' describe where full action potentials are repeatedly generated. If myelin is lost, current can leak away before reaching the next node, potentially slowing or blocking conduction.
| Feature | Unmyelinated axon | Myelinated axon |
|---|---|---|
| Typical propagation | Continuous active regeneration | Active regeneration at nodes plus fast internodal spread |
| Axon insulation | No compact myelin | Compact multilayered myelin |
| Channels needed | Distributed across membrane | Concentrated particularly at nodes |
| Speed at comparable diameter | Usually lower | Usually higher |
| Effect of sheath loss | Not applicable | Can slow or block saltatory propagation |
Separating stimulus size, signal height and firing rate
A sensory input can be stronger without producing a taller action potential in one axon. Greater input often increases firing frequency or recruits additional neurons. The axon carries meaningful patterns through number, timing and frequency of impulses. This avoids the misconception that the membrane potential rises to twice its normal peak whenever a stimulus doubles in strength.
How action potential mechanisms connect to synapses
An action potential arriving at a presynaptic terminal changes its membrane voltage and opens voltage-gated Ca²⁺ channels in many chemical synapses. Calcium entry initiates vesicle fusion and transmitter release, which may create a response in the next cell. The action potential is the long-distance electrical signal within one neuron; synaptic transmission is the transfer of information between cells. The next lesson examines how those events are coupled.
Problem
Axonal region A has just become positive inside, while nearby B remains negative inside. Explain how B becomes active and why A does not normally refire immediately.
- 1.Local axial current from the active A region depolarises adjacent B toward threshold.
- 2.Voltage-gated Na⁺ channels in B open and generate a new action potential.
- 3.Na⁺ channels at A are inactivated during the refractory period and K⁺ currents support recovery, so backward re-excitation is normally prevented.
Quick Quiz
Quiz
Which ion entry produces the fast rising phase of most ordinary neuronal action potentials?
What is repolarisation?
What does threshold mean?
Why is a refractory period important?
What carries local depolarising current toward the next axonal region?
Where is a myelinated axon action potential actively renewed?
What makes saltatory conduction faster than comparable continuous conduction?
If stimulus strength increases above threshold, what commonly changes rather than a single impulse's height?
Practice Problems
- Describe an action potential from threshold through recovery.
- Explain how an action potential travels from region A to B.
- Distinguish absolute from relative refractory periods.
- Compare saltatory and continuous conduction.
- Explain why a stronger stimulus need not produce a taller individual spike.
Adequate depolarisation opens voltage-gated Na⁺ channels, causing rapid inward Na⁺ current and upstroke. Na⁺ channels inactivate and voltage-gated K⁺ channels support K⁺ efflux and repolarisation, sometimes with after-hyperpolarisation, followed by recovery.
Key Takeaways
• An action potential starts when threshold depolarisation opens voltage-gated Na⁺ channels. • Na⁺ entry drives the upstroke, while Na⁺-channel inactivation and K⁺ efflux produce repolarisation. • Local electrical currents trigger action potentials in adjacent axon segments. • Refractory periods help explain why impulses normally propagate away from the initiation region. • Each segment regenerates the signal, preserving action-potential amplitude over distance. • Myelin supports saltatory conduction through rapid internodal spread and node-based regeneration. • Stronger stimuli can raise firing frequency or recruit more axons without making one spike taller.