Nerve Impulses: Sodium, Potassium and Membrane Potential

A thought, a heartbeat, the sting of a paper cut — each is carried by electrical signals travelling along nerve cells. But nerves don’t conduct electricity the way copper wires do, with electrons flowing along a metal. Instead, they use ions crossing membranes through protein channels, creating brief changes in voltage that sweep along the cell. The whole process is electrochemistry, and it can be understood with the same ideas you use for electrochemical cells: concentration gradients, charge separation and equilibrium potentials.

The setup: two gradients

Nerve cells, like all cells, keep very different concentrations of ions inside and outside (typical mammalian values):

Ion	Outside (mmol dm⁻³)	Inside (mmol dm⁻³)
K⁺	5	140
Na⁺	145	12
Cl⁻	110	10
Ca²⁺	2	0.0001

These gradients are built and maintained by the sodium–potassium pump, which uses ATP to move 3 Na⁺ out and 2 K⁺ in on each cycle (see how molecules cross cell membranes and electrolytes in the body). The gradients are the nerve’s “battery”.

The resting potential

At rest, the membrane contains open potassium leak channels, but very few open sodium channels. So the membrane is far more permeable to K⁺ than to Na⁺.

K⁺ ions diffuse out of the cell, down their concentration gradient. Each K⁺ that leaves carries a positive charge, and it leaves behind negative charges — mostly on large proteins and phosphate groups that can’t follow. The inside becomes negative. This growing negative charge starts to pull K⁺ back in. Very quickly, a balance is reached where the electrical pull inward equals the concentration push outward.

The Nernst equation

The voltage at which this balance occurs for a single ion is its equilibrium potential, given by the Nernst equation — the same equation used for electrode potentials in electrochemistry:

E_ion = (RT / zF) ln([ion]_out / [ion]_in)

At body temperature (310 K), RT/F ≈ 26.7 mV, so for a +1 ion:

E = 26.7 mV × ln([out]/[in]) ≈ 61.5 mV × log₁₀([out]/[in])

For K⁺: E_K = 61.5 × log₁₀(5/140) = 61.5 × (−1.447) ≈ −89 mV

For Na⁺: E_Na = 61.5 × log₁₀(145/12) = 61.5 × 1.082 ≈ +67 mV

The real resting potential of a neuron is about −70 mV — close to E_K, because the resting membrane is mostly permeable to potassium, but pulled a little towards E_Na by the small sodium leak. (The Goldman–Hodgkin–Katz equation combines several ions weighted by their permeabilities to predict this value.)

An important point: only a tiny fraction of ions needs to cross to create this voltage. The bulk concentrations barely change. The membrane acts like a capacitor, with a thin layer of excess negative charge inside and positive outside.

The action potential

A nerve impulse, or action potential, is a rapid, temporary reversal of the membrane potential. It depends on voltage-gated ion channels — proteins that open or close in response to the voltage across the membrane.

1. Threshold

A stimulus (for example, neurotransmitter binding at a synapse, or pressure on a touch receptor) makes the inside slightly less negative. If the membrane reaches threshold, typically around −55 mV, voltage-gated sodium channels begin to open.

2. Depolarisation (rising phase)

Na⁺ rushes in, driven both by its concentration gradient and by the negative inside attracting positive ions. This makes the inside more positive, which opens more sodium channels — a positive feedback loop. Within about half a millisecond, the membrane potential shoots up towards E_Na, peaking around +30 to +40 mV. The membrane is now briefly positive inside.

3. Repolarisation (falling phase)

Two things happen at the peak:

• Sodium channels inactivate: a part of the channel protein swings into the pore and blocks it (the “ball-and-chain” mechanism). They can’t reopen until the membrane is negative again.
• Voltage-gated potassium channels open (they respond more slowly). K⁺ flows out, returning the inside to negative.

4. Hyperpolarisation and recovery

Potassium channels close slowly, so the membrane briefly overshoots to around −80 mV, close to E_K. It then returns to the resting potential. During the refractory period — while sodium channels are inactivated — another action potential can’t be triggered (absolutely at first, then only with a stronger stimulus). This makes impulses travel in one direction and limits how fast a nerve can fire.

The whole event lasts about 1–2 milliseconds.

All or nothing

An action potential either happens fully or not at all. A stronger stimulus doesn’t produce a bigger impulse; it produces more frequent impulses. The nervous system encodes intensity as frequency.

Alan Hodgkin and Andrew Huxley worked out this mechanism in the late 1940s and early 1950s using giant nerve fibres from squid, which are wide enough to insert electrodes into. They shared the 1963 Nobel Prize in Physiology or Medicine.

Propagation along the axon

The inward rush of Na⁺ at one point spreads positive charge along the inside of the axon, depolarising the neighbouring membrane to threshold. That region fires, and so on — the impulse travels along the axon like a line of falling dominoes. The refractory region behind it stops it from going backwards.

Myelin: saltatory conduction

Many axons are wrapped in myelin, layers of cell membrane that are rich in lipids (about 70–80 % by dry mass). Being non-polar, myelin is an excellent electrical insulator. It reduces charge leakage and capacitance, so the electrical signal spreads further and faster along the inside. Ion channels are concentrated at gaps in the myelin called nodes of Ranvier, spaced about 1 mm apart. The action potential effectively jumps from node to node — saltatory conduction.

Axon type	Typical speed
Thin, unmyelinated	about 0.5–2 m s⁻¹
Thick, myelinated	up to about 100–120 m s⁻¹

Diseases that damage myelin, such as multiple sclerosis, slow or block conduction.

At the synapse: electrical to chemical

When the impulse reaches the end of the axon, it must cross a gap about 20–40 nm wide to the next cell — the synapse.

1. Depolarisation opens voltage-gated calcium channels. Ca²⁺ flows in (its concentration outside is about 20,000 times higher than inside).
2. Calcium triggers vesicles of neurotransmitter to fuse with the membrane (exocytosis) and release their contents.
3. Neurotransmitter molecules diffuse across the gap and bind receptors on the next cell, opening ion channels there (see neurotransmitters).
4. The neurotransmitter is removed — broken down by enzymes (acetylcholinesterase breaks down acetylcholine) or taken back up by transporters (as with serotonin and dopamine).

Excitatory transmitters (such as glutamate) push the next cell towards threshold; inhibitory ones (such as GABA) pull it away, often by opening Cl⁻ channels.

Chemistry that interferes

Because the action potential depends on specific proteins, many molecules can block it (see venoms and toxins):

• Local anaesthetics such as lidocaine block voltage-gated sodium channels from the inside, stopping pain signals.
• Tetrodotoxin (pufferfish) blocks sodium channels from the outside.
• Some scorpion toxins stop sodium channels inactivating.
• Organophosphate nerve agents and some insecticides inhibit acetylcholinesterase, so acetylcholine builds up and nerves fire uncontrollably.

Common misconceptions

• “Nerves conduct electricity like wires.” The signal is carried by ions crossing membranes, regenerated at each point, not electrons flowing along the axon.
• “Large amounts of Na⁺ and K⁺ swap during an impulse.” Only a tiny fraction moves; the pump restores it over time.
• “The Na⁺/K⁺ pump creates the action potential.” The pump maintains the gradients; channels create the impulse.
• “A stronger stimulus makes a bigger action potential.” It makes more of them, more often.

Key takeaways

• The Na⁺/K⁺ pump builds gradients: K⁺ high inside, Na⁺ high outside.
• The resting potential (~−70 mV) arises mainly from K⁺ leaking out; the Nernst equation gives each ion’s equilibrium potential (E_K ≈ −89 mV, E_Na ≈ +67 mV).
• Voltage-gated Na⁺ channels open at threshold (positive feedback), then inactivate; K⁺ channels repolarise.
• Myelin insulates axons, allowing fast saltatory conduction.
• At synapses, Ca²⁺ triggers neurotransmitter release, turning an electrical signal into a chemical one.