E. Homeostasis · HomeostasisThe Nerve Impulse: Resting Potential and Action Potential
E3.1 E2.1 A1.5 A1.12 A2.2About 75 minutes
Learning goals- I can explain how the sodium–potassium pump and leak channels create a resting membrane potential of about −70 mV.
- I can describe the stages of an action potential and the ion channels involved.
- I can explain threshold, the all-or-none response, refractory periods and how stimulus strength is coded.
- I can explain how myelin and saltatory conduction increase impulse speed and calculate conduction times.
- I can relate disorders and drugs (such as multiple sclerosis and local anaesthetics) to ion channels and myelin.
Words to know
membrane potential
The voltage (charge difference) across a cell membrane, measured inside relative to outside.
resting potential
The membrane potential of a neuron that is not sending an impulse, about −70 mV.
sodium–potassium pump
A membrane protein that uses ATP to move 3 Na⁺ out of the cell and 2 K⁺ in.
depolarization
A change of the membrane potential toward zero or positive values.
threshold
The membrane potential (about −55 mV) at which voltage-gated Na⁺ channels open and an action potential starts.
action potential
A brief, all-or-none reversal of membrane potential that travels along an axon.
refractory period
The short time after an action potential when the membrane cannot fire again (absolute) or needs a stronger stimulus (relative).
saltatory conduction
The jumping of an action potential from node to node along a myelinated axon.
Electricity made of salt
A nerve impulse is electrical, but it is not like a current in a copper wire. No electrons flow down your axons. Instead, the signal is made of ions (charged atoms of sodium and potassium) crossing the membrane through tiny protein gates, one patch of membrane after the next. Understanding this explains why nerve impulses are all-or-none, why they travel in one direction, and how local anaesthetics at the dentist work.
The resting potential: a charged battery
A neuron at rest has a membrane potential of about −70 mV: the inside is negative compared with the outside. Three things create it:
- The sodium–potassium pump. This carrier protein uses ATP (active transport, as you saw in Biochemistry) to pump 3 Na⁺ out for every 2 K⁺ in. So Na⁺ is much more concentrated outside and K⁺ much more concentrated inside. Each cycle also moves one extra positive charge out.
- Leak channels. The resting membrane has many more open K⁺ leak channels than Na⁺ leak channels. K⁺ diffuses out down its concentration gradient, carrying positive charge out, which leaves the inside more negative.
- Large negative molecules (proteins and phosphates) are trapped inside the cell.
The membrane is said to be polarized: charged like a battery, ready to fire.
| Ion | Concentration inside the neuron | Concentration outside | Which way it tends to move if a channel opens |
|---|
| Na⁺ | about 15 mmol/L | about 145 mmol/L | into the cell |
| K⁺ | about 140 mmol/L | about 5 mmol/L | out of the cell |
The action potential, step by step
When a neuron is stimulated (by a receptor or by another neuron), some Na⁺ enters and the membrane depolarizes a little. If the stimulus is too weak, the membrane just returns to rest. But if the membrane reaches threshold (about −55 mV), an action potential fires:
- Depolarization. Voltage-gated Na⁺ channels open. Na⁺ rushes in (down its concentration gradient and attracted to the negative inside). More Na⁺ entering depolarizes the membrane further, which opens more Na⁺ channels: a brief positive feedback loop. The inside shoots up to about +30 to +40 mV.
- Repolarization. Within about a millisecond, the Na⁺ channels inactivate (close and lock), and slower voltage-gated K⁺ channels open. K⁺ flows out, and the inside becomes negative again.
- Hyperpolarization. The K⁺ channels are slow to close, so a little too much K⁺ leaves and the potential briefly dips below −70 mV (to about −80 to −90 mV).
- Return to rest. K⁺ channels close, and the Na⁺/K⁺ pump and leak channels restore the resting potential.
The whole thing takes only about 2 to 3 milliseconds. Very few ions actually cross: the overall concentrations barely change during one impulse. The pump's job is to keep the gradients in place over the long run.
All-or-none, and how strength is coded
An action potential is all-or-none: if threshold is reached, the action potential is always the same size; if not, nothing travels along the axon. So how does your brain tell a gentle touch from a hard pinch? Two ways:
- Frequency: a stronger stimulus produces action potentials more often (more impulses per second).
- Number of neurons: a stronger stimulus activates more neurons (including ones with higher thresholds).
Refractory periods
During the absolute refractory period (while Na⁺ channels are open or inactivated), no new action potential is possible, however strong the stimulus. During the relative refractory period (during hyperpolarization), a stronger-than-normal stimulus is needed. Refractory periods have two important results:
- They limit how often a neuron can fire.
- They make impulses travel in one direction: the patch of membrane behind the impulse is refractory, so the impulse can only move forward.
Propagation
When one patch of membrane depolarizes, positive charge spreads inside the axon to the next patch, bringing it to threshold. That patch fires, and so on, like a row of falling dominoes. In an unmyelinated axon, every bit of membrane must fire in turn, which is slow. In a myelinated axon, the myelin insulates the membrane, and voltage-gated channels are clustered at the nodes of Ranvier. The charge spreads quickly under the myelin, and the action potential seems to jump from node to node: saltatory conduction (from the Latin saltare, to jump). Wider axons also conduct faster.
Worked exampleExample 1: How long does the signal take?
A sensory signal travels 1.0 m from your big toe to your spinal cord. (a) How long does this take in a myelinated axon conducting at 100 m/s? (b) In a thin unmyelinated axon at 1.0 m/s? (c) Explain why you notice a sharp touch on your toe almost at once, but a dull, aching pain can arrive noticeably later.
- (a) t = d ÷ v = 1.0 m ÷ 100 m/s = 0.010 s = 10 ms.
- (b) t = 1.0 m ÷ 1.0 m/s = 1.0 s.
- (c) Touch and sharp pain travel on large myelinated fibres (fast, around tens of ms). Dull, aching pain travels mainly on thin unmyelinated fibres (slow, up to about a second over a long distance). So you sense the sharp signal first and the dull ache arrives later.
(a) 10 ms. (b) 1.0 s. (c) Different fibres: fast myelinated ones carry touch and sharp pain; slow unmyelinated ones carry dull, aching pain.
Worked exampleExample 2: Interpreting the graph
Use the action potential graph. (a) What is the potential at the peak? (b) Approximately how long does the membrane spend above threshold? (c) If the absolute refractory period lasts about 1 ms, what is the theoretical maximum firing rate? Why are real maximum rates lower?
- (a) The peak is about +35 mV.
- (b) The curve crosses −55 mV on the way up at about 1.25 ms and on the way down at about 2.3 ms, so roughly 1 ms.
- (c) If a new action potential can start only every 1 ms at most, the maximum rate is 1 ÷ 0.001 s = 1000 per second.
- Real neurons usually fire much less often (commonly up to a few hundred per second) because the relative refractory period also requires stronger stimuli, and the pumps and channels need time to recover.
(a) About +35 mV. (b) About 1 ms. (c) Theoretical maximum about 1000 per second; real rates are lower.
When signals go wrong, and how drugs use ion channels
- Multiple sclerosis (MS) is an autoimmune disease in which the immune system damages myelin in the CNS. Impulses slow down or fail, causing symptoms such as numbness, vision problems, fatigue or difficulty walking, which often come and go. Canada has one of the highest rates of MS in the world, and Canadian researchers are active in MS research. Treatments can reduce relapses and slow the disease.
- Local anaesthetics such as lidocaine, used by dentists, block voltage-gated Na⁺ channels. With no Na⁺ influx, no action potential can start, so pain signals from that area never reach the brain.
- Tetrodotoxin, a toxin found in pufferfish, also blocks Na⁺ channels, which is why improperly prepared pufferfish can cause paralysis.
- Potassium levels matter: because the resting potential depends on K⁺, abnormally high or low blood K⁺ can disturb nerve and heart function. This links back to why the kidneys (and dialysis) control K⁺ so carefully.
Hands-on activityDomino model of an axon
You need: about 30 dominoes (or identical small books, cards folded into tents, or wooden blocks), a ruler and a flat table.
- Propagation: stand the dominoes in a line about 2 cm apart. Tip the first. Watch the "impulse" travel.
- Threshold and all-or-none: set them up again. Gently nudge the first domino so it wobbles but doesn't fall. What happens to the rest? Now push a little harder until it falls. Does a harder push make the last domino fall any harder? (No: each falls the same way.)
- Refractory period: after they fall, try to send a new impulse from the middle. Which direction can it travel? (Neither, until they are set up again; that's like the refractory period.) Now reset only the first half and push the first domino. Why can't an impulse travel backward into fallen dominoes?
- Speed and spacing: time the fall over the same total length with dominoes 1.5 cm apart and then 3 cm apart (as far apart as still works). Calculate the speed in cm/s for each.
Analyse: For each step, write one sentence that links the model to the real axon (threshold, all-or-none, refractory period, propagation). Then describe one way the model is not like a real axon. (Real axons reset themselves in milliseconds using the Na⁺/K⁺ pump; dominoes need you to reset them. Dominoes use gravity; axons use ion gradients.)
What to look for: a nudge below "threshold" sends nothing down the line; any push that topples the first domino produces the same full wave; fallen dominoes block the wave from going back; the spacing changes the speed of the wave, but the physics of falling dominoes is different from how myelin speeds up a real impulse, so treat this step as a reminder that every model has limits.
Just for funFunny-but-true: Alan Hodgkin and Andrew Huxley worked out how the action potential works by studying the giant axon of the squid, which is up to about a millimetre wide, wide enough to slide a wire inside. They shared the 1963 Nobel Prize in Physiology or Medicine with John Eccles. Modern neuroscience owes a lot to calamari.
Your turn
1What is the approximate resting potential of a neuron?
About −70 mV (inside negative relative to outside).
2Describe what the sodium–potassium pump does.
It uses ATP to pump 3 Na⁺ out and 2 K⁺ in for each cycle, keeping Na⁺ high outside and K⁺ high inside.
3What happens when the membrane reaches threshold?
Voltage-gated Na⁺ channels open, Na⁺ rushes in, and the membrane rapidly depolarizes to about +35 mV: an action potential fires.
4Which ion movement causes repolarization?
K⁺ flowing out through voltage-gated K⁺ channels.
5Explain the all-or-none response.
If threshold is reached, an action potential of full, constant size occurs; if not, no action potential occurs. There are no "half" action potentials.
6How does the nervous system code a stronger stimulus?
By a higher frequency of action potentials and by activating more neurons.
7Why does an impulse travel in only one direction along an axon?
The membrane just behind the impulse is in its refractory period, so it cannot fire again; only the membrane ahead can be brought to threshold.
More practice: warm-up
1Which ion is more concentrated outside a resting neuron?
2What is the threshold potential, approximately?
3What does "saltatory" mean?
Jumping (from node to node).
4Which disease damages myelin in the CNS?
5How do local anaesthetics like lidocaine stop pain signals?
They block voltage-gated Na⁺ channels, so action potentials can't start.
More practice: on your own
1Explain why the inside of a resting neuron is negative even though the pump moves more positive ions out than in only slightly.
Mostly because of K⁺ leak channels: many open K⁺ channels let K⁺ diffuse out, taking positive charge with it, while large negative proteins stay trapped inside. The pump's 3:2 exchange adds a smaller effect and maintains the gradients.
2Describe the role of positive feedback in the rising phase of the action potential.
Depolarization opens some Na⁺ channels; Na⁺ entering causes more depolarization, which opens more Na⁺ channels, so the rise is rapid and self-reinforcing until the channels inactivate.
3A nerve signal travels 0.80 m along a myelinated axon at 80 m/s. How long does it take?
t = 0.80 ÷ 80 = 0.010 s (10 ms).
4Why do impulses in MS sometimes fail completely, not just slow down?
Where myelin is lost, current leaks out of the bare membrane and there are few Na⁺ channels there (they are concentrated at the nodes), so the next node may not reach threshold and the impulse stops.
5A stimulus raises a neuron's membrane potential from −70 mV to −60 mV. What happens? Explain.
No action potential: −60 mV is below threshold (about −55 mV), so voltage-gated Na⁺ channels don't open in enough numbers; the membrane returns to −70 mV.
Challenge
1A drug blocks voltage-gated K⁺ channels but not Na⁺ channels. Predict how the action potential's shape would change and explain.
Depolarization would still occur (Na⁺ channels work), but repolarization would be much slower, relying only on Na⁺ channel inactivation and leak channels. The action potential would be wider (longer), with little or no hyperpolarization, and the neuron could fire less often because recovery is delayed.
2A myelinated axon has nodes 1.0 mm apart. If an impulse takes 0.020 ms to travel from one node to the next, what is the conduction velocity in m/s?
v = d ÷ t = 1.0 × 10⁻³ m ÷ 2.0 × 10⁻⁵ s = 50 m/s.
3If blood K⁺ concentration rises well above normal (hyperkalemia), the concentration gradient for K⁺ across membranes is reduced. Predict the effect on the resting potential and explain why this can be dangerous for heart cells.
With less K⁺ diffusing out, the inside becomes less negative: the resting potential moves closer to threshold (depolarizes). At first cells may become more excitable; if it persists, many Na⁺ channels stay inactivated, so cells may fail to fire properly. In the heart this can cause dangerous irregular rhythms, which is why people with kidney failure must control K⁺ (diet and dialysis).
Quiz
1. The resting potential of a typical neuron is about:
2. The sodium–potassium pump moves:
3. The rising (depolarization) phase of an action potential is caused by:
4. Why can't a second action potential occur immediately after the first?
5. Saltatory conduction occurs in:
6. A stronger stimulus is coded by:
7. Lidocaine works by blocking:
Big idea: a nerve impulse is a wave of ion movement. The Na⁺/K⁺ pump and leak channels charge the membrane (−70 mV); at threshold, Na⁺ rushes in (depolarization), then K⁺ flows out (repolarization). Action potentials are all-or-none, one-way (refractory period) and faster in myelinated axons.
How to help: ask your teen to narrate the action potential graph, phase by phase, saying which channel is open and which way the ions move. The domino model makes threshold and refractory periods concrete.
Common difficulties:
- Thinking ions flow along the axon like electrons in a wire. Ions cross the membrane locally; the signal travels as each patch triggers the next.
- Mixing up the directions. Na⁺ goes in (up), K⁺ goes out (down).
- Thinking the pump causes the action potential. The pump maintains the gradients; channels cause the impulse.