Voltage-gated potassium channel · Grey Matter

The voltage-gated potassium channel is the membrane protein that opens a little after a spike begins and lets potassium flow out, and it is what ends each action potential and sets how fast a neuron can fire again.

Voltage-gated potassium channel. The voltage-gated potassium channel is the membrane protein that opens a little after a spike begins and lets potassium flow out, and it is what ends each action potential and sets how fast a neuron can fire again.

It responds to the same depolarisation as the sodium channel, only more slowly. By the time the voltage peaks, potassium channels are opening; potassium leaves the cell down its gradient, carrying positive charge out, and the voltage falls back toward rest. Many of them stay open a moment longer than needed, so the membrane briefly dips below its resting value (the afterhyperpolarisation) before settling.

Potassium channels are a large family, and their variety is a main reason neurons fire differently. Fast-closing types let a cell fire hundreds of spikes per second (fast-spiking interneurons depend on them); slow, calcium-activated types build up during a burst and make a cell slow down, a property called adaptation.

They are where neuromodulators often act. Closing a resting potassium conductance (as acetylcholine does through muscarinic receptors) makes a cell easier to excite for seconds; opening one (as GABA does through GABA-B receptors) quiets it.

Mutations that weaken some potassium channels raise excitability, and several forms of epilepsy are traced to them.

A spring that snaps a door shut after it is pushed open is the picture of the potassium channel.

Sodium flings the door open, potassium closes it, and how stiff the spring is decides how soon it can be flung again.

Questions: How do potassium channels end each spike and decide how fast a neuron can fire? Voltage-gated potassium channels open a little after the sodium channels, as the spike rises, and the potassium leaving the cell pulls the voltage back down while the sodium channels inactivate. Fast-closing types end the spike quickly and let the cell recover within a millisecond or two, which is how fast-spiking interneurons sustain hundreds of spikes per second. Slower potassium currents, some activated by the calcium that enters with each spike, build up during a train and produce a lasting afterhyperpolarisation, so the cell slows down (adaptation). Which potassium channels a neuron expresses is therefore a large part of its firing personality. Why can a neuron not fire again immediately after a spike, and why does the spike travel only one way? About a millisecond after opening, each sodium channel is plugged by its inactivation gate and stays shut until the membrane has been back near rest for a while, so for that time no input can fire a second spike (the absolute refractory period). Meanwhile potassium channels are still open, holding the voltage low, so for a few milliseconds more only a stronger input succeeds (the relative refractory period). Along the axon, the patch the spike has just left is refractory, so the current can only excite the patch ahead. Together these effects cap the firing rate and make conduction one-way.