The Action Potential and Nerve Conduction

Part 2 · Excitable Tissues · Chapter 6 of 47

Learning objectives

By the end of this page you should be able to:

• Describe the phases of the action potential and the ion channel behind each.
• Explain threshold, the all-or-none law and the positive feedback of the upstroke.
• Distinguish graded potentials from action potentials.
• Explain absolute and relative refractory periods and their consequences.
• Explain how an impulse propagates, and why diameter and myelin set conduction velocity.
• Classify nerve fibres by size and speed.
• Apply these ideas to electrical stimulation, nerve conduction studies, local anaesthesia and demyelinating disease.

Why it matters

Every movement you retrain begins as action potentials in motor nerves. Every sensation you assess arrives as action potentials in sensory nerves. Electrical stimulation, nerve conduction studies and the weakness of multiple sclerosis all make sense only once you know how an impulse is made and carried.

Graded potentials and threshold

Small changes in membrane voltage are called graded potentials. They occur at receptors and synapses, vary in size with the stimulus, and fade as they spread. They can be depolarising (towards zero) or hyperpolarising (more negative).

If a depolarisation reaches threshold, about 15 mV above rest in a typical neuron, something different happens. Voltage-gated sodium channels open in large numbers and an action potential fires.

The phases of the action potential

Figure 1 · The action potential

Depolarisation. At threshold, voltage-gated sodium channels open. Sodium rushes in down both its concentration and electrical gradients, which depolarises the membrane further and opens still more channels. This is positive feedback, and it drives the voltage up within a fraction of a millisecond.

In 1949 Hodgkin and Katz showed that the size of the impulse depends on the sodium concentration outside the axon [2]. The peak approaches, but does not reach, the sodium equilibrium potential from Chapter 5.

Repolarisation. Two things stop the rise. The sodium channels inactivate, closing a second gate that blocks further entry. At the same time, voltage-gated potassium channels, which open more slowly, let potassium flow out.

After-hyperpolarisation. The potassium channels are slow to close, so for a few milliseconds the membrane dips below its resting value before returning.

Figure 2 · Two channels, two timings

In 1952 Hodgkin and Huxley measured these sodium and potassium currents in squid axon and wrote equations that reproduce the action potential from them [1]. Their model remains the foundation of how impulses are understood, and it earned the 1963 Nobel Prize.

Note what the pump does not do. Very few ions cross in a single impulse, so the gradients barely change. The pump restores them over time, but an axon can fire thousands of impulses even with its pumps blocked.

The all-or-none law

Once threshold is reached, the impulse always reaches the same size, whatever the strength of the stimulus. A stronger stimulus does not make a bigger impulse. It makes impulses come more often, and it recruits more fibres. The nervous system codes intensity by frequency and number, not by size.

Refractory periods

Figure 3 · Refractory periods

During the absolute refractory period, the sodium channels are either already open or inactivated. No stimulus can fire another impulse. During the relative refractory period, some sodium channels have recovered but potassium channels are still open, so a stronger stimulus than usual is needed.

Refractoriness has three consequences. It limits the maximum firing rate. It keeps impulses separate. And it makes impulses travel one way, because the membrane just behind an impulse cannot be re-excited.

Propagation along the axon

An action potential in one patch of membrane sends current along the inside of the axon to the next patch. That local current depolarises the neighbouring membrane to threshold, and it fires in turn. The impulse is therefore re-created at each point rather than simply flowing.

Two features speed this up. A wider axon offers less internal resistance, so current spreads further. And myelin, wrapped around the axon by Schwann cells in peripheral nerve and oligodendrocytes in the brain and cord, insulates it.

Figure 4 · Saltatory conduction

In myelinated fibres, sodium channels are packed into the short gaps between myelin segments, the nodes of Ranvier. The impulse is regenerated only at the nodes and current jumps between them. Huxley and Stämpfli provided direct evidence for this saltatory conduction in 1949 [3].

Saltatory conduction is both faster and cheaper, because only the nodes let ions cross and need pumping afterwards.

Nerve fibre types

Two classifications are used. The letter system describes all fibres by size and speed; the Roman numeral system is used for sensory fibres from muscle.

This table explains several clinical observations. The first sharp pain of an injury arrives through Aδ fibres; the later dull ache through C fibres. Touch and vibration travel in large Aβ fibres, which is the basis of the gate control idea behind TENS.

Electrical stimulation

An electrical stimulus applied through the skin moves the membrane of nerves underneath towards threshold. Whether a fibre fires depends on both the current strength and how long each pulse lasts.

The strength–duration curve plots the current needed against pulse duration. Rheobase is the least current that excites with a long pulse. Chronaxie is the pulse duration needed at twice rheobase.

Figure 5 · The strength–duration curve

Nerve has a short chronaxie, so it responds to brief pulses. Denervated muscle, which must be stimulated directly, has a much longer one and needs long pulses. Large-diameter fibres are excited at lower intensity than small ones, which is why sensory TENS can be felt without pain.

Maffiuletti explains that neuromuscular electrical stimulation recruits motor units differently from voluntary effort. Recruitment is non-selective, spatially fixed and temporally synchronous, so stimulated muscle tends to fatigue faster [5]. Current, pulse duration, frequency and duty cycle all need to be chosen with that in mind [5].

Clinical relevance for the physiotherapist

• Multiple sclerosis. Loss of myelin slows or blocks conduction. Some function returns as sodium channels spread along the bare axon, and loss of axons drives lasting disability [4].
• Guillain–Barré syndrome and compression neuropathies. Peripheral demyelination slows conduction velocity, which nerve conduction studies detect.
• Nerve conduction studies. A nerve is stimulated at two points and the time difference converted to a velocity. Typical motor velocities in the arm are around 50–60 m/s in healthy adults.
• Local anaesthetics. They block sodium channels. Small fibres are blocked first, so pain goes before touch and movement.
• Electrotherapy. Pulse duration and intensity determine which fibres fire; NMES fatigues muscle faster than voluntary effort [5].
• Temperature. Cooling slows conduction, which is why limb temperature is controlled in nerve conduction testing and why ice reduces pain transmission.

Assessment and application

Common mistakes

• Saying a stronger stimulus makes a bigger action potential. It makes more of them, more often.
• Crediting the pump with repolarisation. Repolarisation is sodium inactivation plus potassium channels.
• Thinking ions travel along the axon at the speed of the impulse. The impulse is regenerated, not carried.
• Forgetting that myelin is made by Schwann cells peripherally but by oligodendrocytes centrally.
• Assuming NMES recruits motor units like a voluntary contraction [5].

Exam preparation

Long answer

Describe the ionic basis of the action potential. Add a note on saltatory conduction.

• Resting state and threshold.
• Phases with the channel behind each (Figures 1 and 2) [1, 2].
• All-or-none law and positive feedback of the upstroke.
• Refractory periods and their consequences (Figure 3).
• Propagation, myelin, nodes of Ranvier and saltatory conduction (Figure 4) [3].

Short notes

• Refractory periods.
• Classification of nerve fibres.
• Strength–duration curve, rheobase and chronaxie (Figure 5).
• Conduction in demyelinated axons [4].

Viva and practical

• “Why does local anaesthetic abolish pain before touch?” — small fibres are blocked first.
• “Why does denervated muscle need long pulses?” — it has a much longer chronaxie than nerve.
• “Who first described the ionic currents of the impulse?” — Hodgkin and Huxley, 1952 [1].
• OSCE: set up TENS for sensory pain relief and explain the parameters chosen.

Current evidence

Exam and traditional teaching

Demyelination is taught as simple conduction block, and electrical stimulation as recruiting motor units in the same order as voluntary effort.

What the evidence adds

Demyelinated axons can regain conduction by acquiring sodium channels along the exposed membrane, while axon loss, partly driven by sodium entry, underlies lasting disability [4].

Electrically evoked contractions recruit motor units in a non-selective, spatially fixed and synchronous way, which helps explain why they fatigue quickly [5].

What the student should understand

The Hodgkin–Huxley picture explains the impulse. Clinical conditions and electrotherapy are variations on it: change the channels, the myelin or the way the membrane is stimulated, and you change what the patient experiences.

Check yourself

10 questions on this page. Tap one to see the answer and the reasoning.

Quick review

Further reading

References

1. Hodgkin AL, Huxley AF. A quantitative description of membrane current and its application to conduction and excitation in nerve. Journal of Physiology. 1952 Aug;117(4):500–544. doi:10.1113/jphysiol.1952.sp004764 PMID 12991237 Original model
2. Hodgkin AL, Katz B. The effect of sodium ions on the electrical activity of giant axon of the squid. Journal of Physiology. 1949 Mar 1;108(1):37–77. doi:10.1113/jphysiol.1949.sp004310 PMID 18128147 Experimental study
3. Huxley AF, Stämpfli R. Evidence for saltatory conduction in peripheral myelinated nerve fibres. Journal of Physiology. 1949 May;108(3):315–339. PMID 18144923 Experimental study
4. Waxman SG. Axonal conduction and injury in multiple sclerosis: the role of sodium channels. Nature Reviews Neuroscience. 2006 Dec;7(12):932–941. doi:10.1038/nrn2023 PMID 17115075 Review
5. Maffiuletti NA. Physiological and methodological considerations for the use of neuromuscular electrical stimulation. European Journal of Applied Physiology. 2010;110(2):223–234. doi:10.1007/s00421-010-1502-y PMID 20473619 Review

Related topics

• Previous: Chapter 5 — The Resting Membrane Potential
• Next: Chapter 7 — The Synapse and the Neuromuscular Junction
• Electrotherapy
• Multiple sclerosis physiotherapy

Reviewed by the Physiotherapist India Team. · Human Physiology contents