Ion Channel Biophysics

Hodgkin-Huxley Action Potential

The full ionic model: voltage-gated Na+ and K+ channels with gating variables (m, h, n), pharmacological blockade (TTX, TEA), and clinical correlates from pufferfish poisoning to demyelination.

Presets

Stimulus

Conductances

Reversal Potentials

Pharmacology

Membrane voltage

Action Potential Waveform

resting (-65 mV)0 mVTime (ms)

Summary

Spike metrics

Spikes

1

Peak voltage

39.4 mV

Na+ block

0%

K+ block

0%

Pharmacology

No pharmacological blockade applied.

Action potential phases

Resting

Membrane sits near -65 mV, set by K+ leak and the Na+/K+ ATPase. Gates: m low, h high, n moderate.

Depolarization

Stimulus raises V past threshold → m gates open fast → Na+ rushes in → positive feedback drives the upstroke to ~+40 mV.

Repolarization

h gates close (Na+ inactivation) while n gates open (delayed K+ rectifier) → outward K+ current pulls V back down.

Undershoot

K+ channels are still open after Na+ channels close → V dips below resting (afterhyperpolarization) before n gates relax.

Recovery

h gates de-inactivate and n gates close → membrane returns to resting, ready for the next spike.

What to notice

  • The model produces 1 spike with a peak of 39.4 mV.
  • Watch the gating variables: m (fast activation) leads, h (inactivation) follows, n (K+ activation) is slowest.
  • The Na+ current (blue) is brief and large; the K+ current (red) is slower and sustains repolarization.
  • The afterhyperpolarization sets the relative refractory period: another spike requires stronger stimulus during this window.

Biological analogies

gNa

Density of voltage-gated Na+ channels. Reduced in demyelination or by TTX/local anesthetics.

gK

Density of delayed-rectifier K+ channels. Blocked by TEA and 4-aminopyridine.

gL

Background leak conductance. Increases with membrane damage or demyelination.

m gate

Na+ activation — opens within ~0.1 ms of depolarization. The fastest gate.

h gate

Na+ inactivation — closes with ~1 ms delay, creating the absolute refractory period.

n gate

K+ activation — opens with ~1 ms delay, drives repolarization and the afterhyperpolarization.

TTX

Tetrodotoxin (pufferfish toxin) — plugs Na+ channel pore from outside. Also models lidocaine mechanism.

TEA

Tetraethylammonium — blocks K+ channels from outside. Reveals the Na+ component in isolation.