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The action potential: the same size, however hard you push

A neurone at rest is holding a battery charged, at a cost of about a fifth of a cell's ATP. The impulse is that battery being discharged and recharged in a millimetre of membrane at a time, over and over, along the length of the axon.

Before this Receptors, transducers and the generator potential · Facilitated diffusion and active transport

Before you start

The impulse travels along the neurone like electricity down a wire. It is a comfortable picture and it is wrong in a way that costs marks all the way through this topic. Nothing flows along the axon. What moves is a sequence of events across the membrane: ions crossing at one point, depolarising the patch next door, which then does the same to its neighbour. Electricity in a copper wire manages about two thirds of the speed of light; the fastest human axon manages about 100 m s⁻¹, which is roughly a millionth of that. The impulse is a wave of depolarisation, and it has to be rebuilt at every step.

What you should be able to do

Explain how the sodium-potassium pump and the membrane's permeability produce a resting potential of about −70 mV.
Describe depolarisation, repolarisation and hyperpolarisation in terms of which gates are open.
State the all-or-nothing principle and say what does vary with stimulus strength.
Explain the refractory period and give its three consequences.
Account for conduction speed using myelination, axon diameter and temperature.

Holding a charge: the resting potential

An axon that is doing nothing is not doing nothing. Its inside sits at about −70 mV relative to the outside, and holding it there takes continuous work.

The work is done by the sodium-potassium pump, a carrier protein that hydrolyses ATP to move three sodium ions out for every two potassium ions in. Both are moved against their concentration gradients, so this is active transport. Notice the arithmetic: three positive charges leave for every two that enter, so each cycle makes the inside slightly more negative.

That alone would only account for a few millivolts. Most of the resting potential comes from the membrane's differential permeability. The membrane has many potassium channels open at rest and very few sodium channels, so it is far more permeable to potassium than to sodium. Potassium therefore leaks back out, down the steep gradient the pump has just built, taking positive charge with it. Sodium cannot leak back in at anything like the same rate. Add the large negatively charged proteins and organic anions trapped inside the axon, which cannot cross at all, and the inside settles at about −70 mV.

Resting potential: The potential difference across the membrane of a neurone that is not conducting an impulse, about −70 mV inside relative to outside.
Polarised: Describes a membrane with a potential difference across it; at rest the axon membrane is polarised with the inside negative.
Voltage-gated channel: A channel protein that opens or closes in response to a change in the potential difference across the membrane.

One consequence is worth holding on to: an axon at rest has a store of potential energy in two ion gradients, and it has paid for that store in ATP. Nervous tissue is expensive to run — the brain uses about a fifth of a resting person's energy — and most of that bill is this pump.

One millisecond, four phases

Bring the membrane to about −55 mV, by whatever means, and the response stops being proportional and becomes automatic. The voltage-gated sodium channels open, and everything that follows is a consequence.

Watch the gates rather than the line. Every feature of the trace — the steep rise, the fall, the dip below the resting value — is a statement about which channels are open at that instant.

Depolarisation. Voltage-gated sodium channels open and sodium ions rush in, down both their concentration gradient and the electrical gradient. The inside becomes less negative, which opens more sodium channels, which lets in more sodium: positive feedback, and the reason the rise is so steep. The potential overshoots zero and reaches about +40 mV.

Repolarisation. At the peak the sodium channels close — they inactivate automatically after about half a millisecond — and the voltage-gated potassium channels, which are slower to respond, are by now open. Potassium ions leave, carrying positive charge out, and the potential falls back towards its resting value.

Hyperpolarisation. The potassium channels are slow to shut as well as slow to open, so potassium keeps leaving after the resting value has been passed. The inside overshoots to about −80 mV before the channels finally close and the sodium-potassium pump restores the resting potential.

The same events plotted once, with the phases coloured. If you are asked to label a trace, the two things to get right are the value at the peak and the fact that the line dips below the resting potential before it recovers.

The whole event takes about a millisecond. Only a tiny fraction of the axon's ions actually move — a squid axon can fire thousands of times before the gradients run down noticeably — which is why the pump can catch up between impulses rather than having to keep pace with each one.

All-or-nothing, and what varies instead

Below threshold, nothing happens: the small depolarisation fades and no impulse is produced. At or above threshold, a full action potential occurs, and it is identical whatever the stimulus. A stimulus a hundred times threshold produces exactly the same +40 mV peak as one just over it. This is the all-or-nothing principle, and it follows from the mechanism: once enough sodium channels have opened, the positive feedback runs to completion on its own.

Which raises the obvious question. If every impulse is the same, how does your nervous system distinguish a tap from a punch?

Two answers, both visible here. A stronger stimulus produces impulses more often in a given neurone, and it also recruits more neurones — the figure shows the first.

Stimulus intensity is coded in two ways, and a full-mark answer gives both. The frequency of impulses along a neurone rises with the strength of the stimulus, and the number of neurones firing rises too, as receptors with higher thresholds are brought in. Nothing about the amplitude changes, ever.

Reading a trace from an experiment

A student records from a single sensory neurone. With a stimulus of 2 units they record 15 impulses in a second; with 6 units they record 45 impulses in a second, each of the same amplitude. A classmate says the second stimulus produced 'three times the signal'. Is that a fair description?

It is fair about the message and wrong about the mechanism, so it needs unpicking. The frequency has tripled, from 15 Hz to 45 Hz, and frequency is exactly how intensity is coded, so the nervous system does receive a stronger message.

But each impulse is unchanged: same peak, same duration, same shape. Nothing is three times bigger. Writing 'the action potentials were larger' would contradict the data the student collected.

There is also a ceiling implied by these numbers. The refractory period sets a minimum interval between impulses, so above some stimulus strength the frequency in this one neurone cannot rise further, and any further increase has to be reported by recruiting other neurones.

The refractory period, and the three things it does

For a short time after an action potential the membrane cannot produce another. During the absolute refractory period the sodium channels are inactivated and no stimulus of any size will do anything; during the relative refractory period that follows, the membrane is hyperpolarised and only an unusually strong stimulus will work. Together they last a millisecond or two.

Three consequences follow, and they are worth learning as a set because questions ask for them as one.

Impulses stay discrete. One action potential cannot merge into the next, so a train of impulses arrives as separate events that can be counted — which is what makes frequency usable as a code in the first place.

Impulses travel in one direction. The patch of membrane behind the impulse has just fired and is refractory, so it cannot be depolarised again by its neighbour. The only membrane available to depolarise is the patch ahead, and the wave moves forwards.

There is an upper limit on frequency. If the refractory period lasts about 2 ms, the neurone cannot fire more often than about 500 times a second, which caps how intense a stimulus a single neurone can report. Beyond that, the extra information has to come from other neurones joining in.

How fast, and what changes it

Conduction speed varies enormously between neurones — from under 1 m s⁻¹ to about 100 m s⁻¹ — and three factors account for the range.

Myelination. Schwann cells wrap themselves round an axon many times, and the layers of membrane act as an electrical insulator. Ions cannot cross where the myelin is, so depolarisation can only happen at the nodes of Ranvier, the gaps between adjacent Schwann cells, spaced every millimetre or so. The local currents therefore flow from node to node and the impulse jumps the insulated stretches between them. This is saltatory conduction, and because far fewer patches of membrane have to be depolarised, it is dramatically faster.

Both axons are the same length. Count the places that have to depolarise in each: nineteen on the bare axon, five on the myelinated one. That difference is the whole of saltatory conduction.

Axon diameter. A wider axon offers less resistance to the flow of ions along its length, so local currents spread further and depolarise the membrane ahead more quickly. There is also proportionally less leakage of charge across the membrane. Invertebrates without myelin reach useful speeds by brute force: the squid's giant axon, which is about a millimetre across, exists to make its escape response fast enough to be worth having.

Temperature. Ions diffuse faster when warmer, and the pump and channel proteins work faster too, so conduction speeds up as temperature rises — until roughly 40 °C, above which the proteins begin to denature and conduction fails. This is why an ectotherm is sluggish on a cold morning and why experiments on nerve speed always state the temperature.

Factor	Effect on speed	Why
Myelination	Up to about 100 m s⁻¹, against about 1 m s⁻¹ without	Depolarisation only at the nodes: saltatory conduction
Axon diameter	Wider is faster	Less resistance to ion flow along the axon, less leakage
Temperature	Faster when warmer, up to about 40 °C	Faster diffusion and faster carrier proteins; denaturation above

TRY IT — Explaining a symptom from the biology

In multiple sclerosis the immune system destroys patches of the myelin sheath around axons in the central nervous system. Suggest why this produces slowed and unreliable responses.

Check your answer

Without myelin over a stretch of axon, saltatory conduction is lost there. The impulse can no longer jump from node to node, so every patch of membrane along the damaged stretch has to be depolarised in turn, and conduction along it slows towards the 1 m s⁻¹ of an unmyelinated axon.

Responses that depend on those neurones are therefore delayed, and because the delay differs from axon to axon, signals that should arrive together no longer do — which affects coordination and balance as much as it affects speed.

Where the damage is severe, local currents may not depolarise the next node to threshold at all, and the impulse fails completely. That is why the effects range from mild slowing to loss of function, depending on how much of the sheath has gone.

In the exam

Say sodium and potassium, not 'ions'. Almost every mark in this topic is for naming which ion moved, which way, and through what.
The pump moves three sodium out for two potassium in, and it uses ATP. Quote the ratio: it is a mark on its own and it explains the sign of the resting potential.
'Depolarisation' means the inside becomes less negative. It does not mean the impulse. Questions that ask you to describe an action potential want the gates named in order.
Never write that a bigger stimulus gives a bigger action potential. Intensity is coded by frequency of impulses and by the number of neurones firing.
For saltatory conduction, say that depolarisation occurs only at the nodes of Ranvier and that the impulse jumps between them. 'The myelin makes it faster' on its own is not an explanation.
If a question gives you a temperature or an axon diameter, it wants that factor used. Data in the stem is there to be quoted back.

Check yourself

A neurone is treated with a drug that blocks voltage-gated potassium channels but leaves the sodium channels and the sodium-potassium pump working. Predict the effect on the shape of an action potential in that neurone, and explain each part of your prediction.

Answer

The rising phase would be unchanged. Depolarisation depends on voltage-gated sodium channels opening and sodium ions entering, and neither is affected, so the membrane would still reach about +40 mV at the same rate.

Repolarisation would be much slower. Normally potassium ions leave through the voltage-gated potassium channels, carrying positive charge out and bringing the potential down quickly. With those channels blocked, the fall would depend on the pump and on whatever leakage remains, both far slower, so the action potential would be prolonged.

The hyperpolarisation would be reduced or absent altogether. The undershoot exists because potassium continues to leave after the resting value is passed, and if that exit is blocked there is nothing to carry the potential below −70 mV.

One knock-on effect is worth adding: a prolonged action potential lengthens the refractory period, so the neurone could not fire as often. Its maximum frequency would fall, and with it the intensity of stimulus it can report.

Questions

Written to the command words the boards use. Try them on paper before opening a scheme: the marks go to points made, not to length.

Question 14 marks

Explain how the sodium-potassium pump and the permeability of the axon membrane together establish a resting potential of about −70 mV.

Mark scheme

B1 the pump hydrolyses ATP to move three sodium ions out for every two potassium ions in, both against their concentration gradients
B1 three positive charges leave for every two that enter, so each cycle of the pump makes the inside slightly more negative
B1 the membrane has many potassium channels open at rest and very few sodium channels, so it is far more permeable to potassium than to sodium
A1 potassium therefore leaks back out down the steep gradient the pump has built, carrying positive charge with it, while large negatively charged proteins are trapped inside and cannot leave

Question 24 marks

Describe the changes in membrane potential during an action potential, from threshold to the recovery of the resting value, in terms of which voltage-gated channels are open at each point.

Mark scheme

B1 at about −55 mV voltage-gated sodium channels open and sodium ions diffuse in, so the inside becomes less negative
B1 the depolarisation opens more sodium channels, which is positive feedback, and the potential overshoots zero to reach about +40 mV
B1 at the peak the sodium channels inactivate and the slower voltage-gated potassium channels are now open, so potassium leaves and the potential falls back: repolarisation
A1 the potassium channels are slow to shut, so potassium keeps leaving past the resting value to about −80 mV, and the sodium-potassium pump then restores the resting potential

Question 34 marks

Explain what is meant by the all-or-nothing principle, and explain how the nervous system distinguishes a light touch from a heavy blow if every action potential is the same size.

Mark scheme

B1 below threshold no action potential is produced at all, and the small depolarisation simply fades away
B1 at or above threshold a full action potential occurs and reaches the same peak of about +40 mV whatever the size of the stimulus, because the positive feedback runs to completion on its own
B1 a stronger stimulus increases the frequency of impulses along a neurone
A1 a stronger stimulus also recruits more neurones, as receptors with higher thresholds are brought in, and nothing about the amplitude of any impulse changes

Question 44 marks

Explain what causes the refractory period after an action potential, and explain two consequences it has for the impulses a neurone can carry.

Mark scheme

B1 during the absolute refractory period the voltage-gated sodium channels are inactivated, so no stimulus of any size can produce another action potential
B1 during the relative refractory period that follows the membrane is hyperpolarised, so an unusually strong stimulus is needed
B1 the patch of membrane behind the impulse has just fired and is refractory, so only the membrane ahead can be depolarised and the impulse travels in one direction
A1 the refractory period sets a minimum interval between impulses, so it keeps them as separate countable events and puts an upper limit on the frequency a single neurone can reach

Question 54 marks

An action potential is recorded 8.4 cm along an axon from the point of stimulation, 1.2 ms after the stimulus was applied. Calculate the conduction velocity of this axon in metres per second, and calculate how long an impulse would take to travel 1.4 m along an unmyelinated axon conducting at 1.0 m s⁻¹.

Mark scheme

M1 velocity is distance divided by time, with both converted to metres and seconds: 8.4 cm is 0.084 m and 1.2 ms is 1.2 × 10⁻³ s
A1 0.084 ÷ 0.0012 gives a conduction velocity of 70 m s⁻¹
M1 time is distance divided by velocity, so 1.4 ÷ 1.0
A1 1.4 s, which is more than a thousand times the 20 ms the myelinated axon would take over the same distance

Question 63 marks

A local anaesthetic injected at a tooth blocks the voltage-gated sodium channels in the sensory neurones nearby. Suggest why the patient feels no pain from the tooth, and suggest why the sense of touch in the lip on that side is lost as well.

Mark scheme

B1 with the voltage-gated sodium channels blocked, sodium ions cannot rush into the axon, so the membrane cannot depolarise to +40 mV and no action potential is generated
B1 no impulses therefore reach the brain from the receptors in the tooth, and pain is only felt when impulses arrive there
B1 the drug cannot distinguish one neurone from another, so it blocks the channels in every axon it reaches, including those carrying impulses from touch receptors in the lip

Question 72 marks

State the resting potential of a typical neurone in millivolts, and state the ratio in which the sodium-potassium pump moves the two ions across the membrane.

Mark scheme

B1 the resting potential is about −70 mV, with the inside negative relative to the outside
B1 the pump moves three sodium ions out for every two potassium ions in

Worth remembering

Resting potential is about −70 mV, held by a 3:2 pump and a membrane far more permeable to potassium than to sodium.
Sodium in for the rise, potassium out for the fall, potassium slow to shut for the undershoot.
All action potentials in a neurone are the same size; intensity is frequency and neurone number.
The refractory period keeps impulses discrete, keeps them one-way, and caps their frequency.
Myelinated and wide and warm is fast; bare and thin and cold is slow.

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