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
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.