Why are potassium channels slower than sodium channels?

Question

I am relatively new in the subject of biology. I have a strong mathematical background and in order to get into the field of computational neuroscience, I am trying to get some biological background.

I am reading about the general mechanism of action potentials in neurons. I understand that an action potential starts with a fast entrance of sodium into the postsynaptic cell. Since the potassium channels are slower than the sodium channels, potassium starts flowing out of the cell only around the peak of the action potential, thereby hyperpolarizing the cell's membrane potential.

What is the mechanism that causes the potassium channels to activate slower than the sodium channels? Does it involve differences in the behavior of the suitable neurotransmitters? Because I didn't manage to find transmitters or couples of transmitters and receptors which activate potassium channels, but not sodium channels (or sodium channels and not potassium channels).

Answer 1

Short answer
The activation kinetics of Na⁺ channels are faster than K⁺ channels.

Background
Voltage-dependent channel gating basically occurs through three possible states of the channel: open, closed and inactivated (Fig. 1).

^{Fig. 1. Gating of a voltage-activated sodium channel. Source: Balseiro Institute.}

Basically, ion channels are protein pores in the membrane. Upon depolarization, the pore opens, which is a process with fast kinetics in Na⁺ channels and slower kinetics in K⁺ channels (Lacroix et al, 2013). K⁺ channel activation is in the order of 6 times slower than Na⁺ channel activation. The slower inactivation of K⁺ channels allows sufficient Na⁺ to flow in the cell for the depolarization phase of the action potential to develop (Fig. 2).

^{Fig. 2. Action potentials and underlying Na+ and K+ currents. Source: Dundee Med Student Notes.}

After opening, the channel is inactivated, which can occurs through a physical "protein-plug" as shown in Fig. 1, or through conformational changes in the pore. This inactivation again is fast in Na⁺ channels leading to a transient spike in the action potential, and deactivation is slower for K⁺ channels (K⁺ channels do not inactivate, but rather deactivate). This inactivation step results in the refractory period of a neuron (silent period after firing). The channel is then de-inactivated and converted to the closed state, after which the channel is again ready to participate in another round of firing.

Note that neurotransmitters do not activate voltage-gated channels directly. Neurotransmitters can activate ion channels, but those are ligand-gated ion channels, such as the nicotinergic acetylcholine receptor, AMPA receptor or NMDA receptor (Purves et al., 2001).

<sup>References
- Lacroix et al, Neuron (2013); 79(4): 651-7
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates (2001)</sup>