Action Potentials Tournament
Two onboarding diagrams orient you in the ion-channel landscape of the neuron. Then eight MCAT-DoK quiz rounds: why the resting potential sits near E_K, Nav activation vs. inactivation gates, the full spike sequence, a Nernst calculation, absolute vs. relative refractory periods, graded EPSPs vs. all-or-none spikes, tetrodotoxin and local anesthetics, and why demyelination in multiple sclerosis slows conduction.
Where the Potassium channels fits in Neuronal system
Reactome's Neuronal System map collects the ion-channel families that make a neuron electrically excitable - the voltage-gated Na+, K+, and Ca2+ channels plus the ligand-gated receptors of the synapse. Every action potential is written by a race between two of those families: Nav channels drive the upstroke, and the highlighted voltage-gated potassium channel panel is the family that repolarizes the membrane and carves out the hyperpolarizing undershoot. Click the highlighted Potassium channels panel to enter the tournament.
Click the highlighted Potassium channels box to continue.
What this tournament tests
Each task maps to a distinct MCAT cognitive demand. The first two orient you in the broader topology; the next eight test the high-yield mechanism, regulation, sequence and quantitative reasoning that consistently appear on test day.
The Bigger Picture
Anchor voltage-gated potassium channels inside the neuronal system on the live Reactome map.
Whole-Pathway Overview
Pan and zoom the curated WikiPathways voltage-gated sodium channel figure before you start answering.
Fill in the Blank
Recall that open K+ leak channels are why the resting potential sits near E_K, not midway to E_Na.
Disruptor
Predict why tetrodotoxin abolishes the spike while leaving the resting potential intact.
Sequence Ordering
Trace threshold -> Nav activation -> overshoot -> Nav inactivation -> Kv repolarization -> undershoot -> rest.
Match the Pairs
Pair each player (Na+/K+ ATPase, K+ leak, Nav, Kv, tetrodotoxin, lidocaine, nodes of Ranvier) with its exact role.
Numeric Input
Compute E_K from the Nernst equation with physiologic K+ concentrations.
Select All That Apply
Identify TRUE statements about Nav gating states, absolute vs. relative refractory periods, and hyperkalemia.
Odd One Out
Separate graded, decremental signals (EPSP, IPSP, receptor potential) from the all-or-none action potential.
Demyelination Disruptor
Explain why multiple sclerosis slows conduction through lost membrane resistance and added capacitance.
Public leaderboard
Your score posts to a global, persistent leaderboard scored by points first, time as tiebreaker.
Action potentials in 60 seconds
The resting membrane potential (about -70 mV) exists because the membrane is selectively permeable. K+ leak channels are open at rest, so Em is pulled close to E_K (about -90 mV), while the Na+/K+ ATPase (3 Na+ out, 2 K+ in per ATP) maintains the gradients and adds a few millivolts of electrogenic hyperpolarization. Equilibrium potentials come from the Nernst equation, E = (61/z) log10([out]/[in]); the real Em is a weighted average of E_K and E_Na set by relative permeability.
Graded depolarizations summate at the axon hillock. If they reach threshold (about -55 mV), voltage-gated Na+ channel activation gates open and Na+ influx becomes self-reinforcing - the spike is all-or-none. Near the peak the slower inactivation gate shuts (absolute refractory period) while delayed Kv channels open, so K+ efflux repolarizes the membrane. Sluggish Kv closure overshoots into a hyperpolarizing undershoot toward E_K. Threshold -> upstroke -> inactivation -> repolarization -> undershoot -> rest.
Refractory periods matter twice: the absolute refractory period (Nav inactivated, resettable only by repolarization) enforces one-way propagation and caps firing frequency, while the relative refractory period lets a stronger stimulus fire early. Because amplitude is fixed, stimulus intensity is encoded as firing frequency and fiber recruitment. Conduction velocity rises with axon diameter and with myelination, which produces saltatory conduction between nodes of Ranvier.
High-yield perturbations: tetrodotoxin and saxitoxin plug the Nav pore from outside, and lidocaine blocks Nav use-dependently from inside (small pain fibers first). Hyperkalemia makes E_K less negative, depolarizing Em - first hyperexcitable, then weak as Nav channels sit inactivated - while hypocalcemia lowers threshold and causes tetany. Multiple sclerosis (CNS oligodendrocytes) and Guillain-Barre syndrome (PNS Schwann cells) slow or block conduction by destroying myelin, not by destroying the pump.
FAQ
Why is the resting potential -70 mV and not -90 mV?
E_K is about -90 mV, and K+ leak channels dominate resting permeability, so Em starts close to E_K. But the membrane is not perfectly K+ selective: a small resting Na+ permeability leaks positive charge inward and drags Em up toward -70 mV. The Na+/K+ ATPase contributes a few extra millivolts of hyperpolarization because it exports 3 Na+ for every 2 K+ it imports.
What actually makes an action potential all-or-none?
Positive feedback. Na+ entry depolarizes the membrane, which opens more voltage-gated Na+ channels, which admits more Na+. Once threshold is crossed, that loop runs to completion independent of the original stimulus, so every spike in a given axon has the same amplitude. Stimulus intensity is therefore encoded as firing frequency and by how many axons are recruited, never as spike height.
How do the two Na+ channel gates differ?
The activation gate is closed at rest and opens within a fraction of a millisecond when the membrane depolarizes past threshold. The inactivation gate is open at rest and closes a bit later, plugging the pore from the cytoplasmic side. Because only repolarization resets the inactivation gate, no stimulus - however strong - can fire a second spike during the absolute refractory period.
Why does myelin speed conduction up so much?
Myelin increases membrane resistance and decreases membrane capacitance, so injected current is funneled longitudinally down the axoplasm instead of leaking across the membrane. The spike is only regenerated at the Nav-dense nodes of Ranvier, jumping node to node - saltatory conduction. Demyelination in multiple sclerosis adds capacitance and leak, so depolarization dies out before it reaches the next node.
Do I need an account to play?
No. The tournament is fully public. You get a randomized handle and your score posts to the public leaderboard at the bottom of this page.
Keep going
What happens once the spike reaches the axon terminal - Ca2+ influx, SNARE-mediated vesicle fusion, and receptor binding.
Excitation-contraction coupling - how the sarcolemmal action potential becomes SR Ca2+ release and cross-bridge cycling.
Overview diagram: Reactome Pathway R-HSA-112316, licensed CC BY 4.0.