Action Potentials and Conduction

A fast activation gate (m) that opens on depolarisation in ~0.1–0.5 ms, and a slower inactivation gate (h) that closes on depolarisation in ~1 ms. In series, they make the channel self-terminating.

Naᵥ opening is regenerative positive feedback; once threshold (~−55 mV) is crossed the spike proceeds, and its amplitude is set by the ion gradients, not stimulus strength. Information is coded in frequency, not amplitude.

The voltage (~−55 mV) at which inward Na⁺ current just exceeds outward K⁺/leak current, triggering the regenerative loop.

Naᵥ inactivation and slow Kᵥ-mediated K⁺ efflux are already occurring, so V_m never fully approaches E_Na.

Kᵥ channels close sluggishly, so g_K remains above resting level and V_m drifts toward E_K (−90 mV) before settling back.

No. One action potential moves only ~10⁻¹² mol/cm² of ion — negligible. The pump maintains gradients long-term; repolarisation is done by K⁺ efflux through Kᵥ channels.

Absolute: Naᵥ h-gates are inactivated, no stimulus of any strength can fire a spike. Relative: during afterhyperpolarisation some h-gates have reset but g_K is high and V_m is further from threshold, so a stronger-than-normal stimulus is needed.

(1) Action potentials cannot summate or tetanise (vital for cardiac filling); (2) propagation is unidirectional because the membrane behind the spike is inactivated. It also caps firing at ~500–1000 Hz.

λ = √(r_m/r_i): the distance passive current spreads before decaying. It increases with membrane resistance (r_m) and decreases with axoplasmic resistance (r_i).

τ = r_m·c_m, the time for a patch to charge. Conduction velocity rises with a larger λ and falls with a longer τ.

By local circuit currents: the depolarised patch acts as a current source, positive charge flows longitudinally through axoplasm to the adjacent resting patch, bringing it to threshold.